1. Fibrocartilaginous Embolism (FCE)

Fibrocartilaginous embolism (FCE) causes peracute to acute paralysis by occluding arterial or venous blood vessels in the spinal cord with fibrocartilaginous material leading to sudden ischemia and consequently to neurological deficits. Depending on size and location of the affected blood vessels, different neurological symptoms may develop. FCE has a high prevalence in young adult to middle-aged dogs of larger breeds (80% weigh 20–25 kg or more), even though it may affect any breed at nearly any age. However, two smaller breeds, the Sheltie and the Miniature Schnauzer, may be more often affected than other small-breed dogs. Clinical history includes sudden paralysis during exercise (playing, jumping, running). Many patients cry out in pain in the initial moment, but they are non-painful once they are presented to the veterinarian. Neurological signs may progress within the first 24 hours in some cases, but usually progression is restricted to the first minutes or the first hour. Depending on the location of the embolism along the spine, only rear limbs or all four limbs may be affected. Lesion distribution along the spine is as follows: nearly 50% patients: lumbar intumescence (L4-S3); one third of the patients: cervical intumescence (C6-Th2); and some cases in C1-5 and Th3-L3. In many cases, neurological signs are asymmetric to a degree, which would not be likely with a compressive spinal cord lesion. The severity of neurological deficits may vary from mild ambulatory paresis to paraplegia without deep pain perception. There is no test to diagnose FCE with certainty in vivo. However, ruling out other potential causes may allow a very likely presumptive diagnosis. The one single test to diagnose the disease would be spinal MRI, where a typical intraspinal signal hyperintensity can be seen on T2 weighted images. However, establishing a strong presumptive diagnosis MRI may not really be necessary. It is sufficient, to rule out any compressive lesion using myelography in a patient with typical signalment and clinical history.

Therefore, the following approach can be recommended. FCE is very likely if the following criteria are fulfilled: young adult to middle-aged large-breed dog, acute paralysis during exercise, no progression of clinical signs beyond the first hour, no pain on spinal palpation, no extradural compression on myelography. There is no specific treatment beside supportive care and physiotherapy. Anecdotally, FCE has been treated using propentofylline at a dose of 3 mg/kg BID. In general, prognosis is usually fair with two thirds of dogs recovering. Significant improvement is usually seen within two weeks. Negative prognostic indicators are: bilateral neurological deficits, involvement of lower motor neurons, plegia without deep pain perception.

2. Acute Vestibular Disturbances in Old Dogs

Vestibular disturbances are probably one of the most incapacitating problems owners may have to encounter in their dogs. However, the most common causes of acute vestibular signs in geriatric dogs are non-neoplastic, potentially curable diseases such as idiopathic old dog vestibular disease; hypothyroidism and brain infarction. A thorough neurological examination should allow differentiating those diseases from other intracranial lesions.

Idiopathic (Geriatric) Vestibular Disease

This disease does usually affect medium-sized and large-breed dogs from 10 years of age on. The clinical symptoms, appearing acutely or peracutely, are those of a peripheral vestibular disease: severe generalized but asymmetric ataxia, head tilt, circling to the same side as the head tilt and horizontal or rotatory nystagmus with the fast phase away from the tilted side. Sometimes, more severe signs such as falling and rolling as well as vomiting may be seen. In idiopathic old dog vestibular disease, the patient should not have any other than the described vestibular deficits. Specifically, there should neither be another cranial nerve involvement nor conscious proprioceptive deficits. Currently, there is no treatment known to alter the course of the disease. However, in patients with severe nausea, central acting antiemetic medication might be helpful during the first days: meclizine 25 mg per dog PO SID (anti-histamine; H1 receptor), maropitant 1 mg/kg SC SID (NK-1 receptor blocker), promethazine 0.2–2 mg/kg PO SID (anti-histamine; H1 receptor). In some cases intravenous fluid support is necessary, since patients may not drink or may not be able to drink sufficiently. Usually clinical signs improve with 3 to 4 days starting with diminishing of the nystagmus. However, complete recovery may take up to 3 weeks. In some cases, a slight residual head tilt may persist. Relapses are unusual, but they can be seen in some rare cases.

Hypothyroidism

Neurological deficits may be seen in combination with generalized signs of reduced thyroid function (lethargy, exercise intolerance, alopecia, dry skin and weight gain) or they may be the only manifestation of hypothyroidism. Acute vestibular signs may be combined with other neurological deficits including laryngeal and facial paralysis, megaesophagus or rear limb weakness. However, more frequently, vestibular deficits are the only manifestation of the disease. Hypercholesterolemia and hypertriglyceridemia on initial blood chemistry screening should arouse suspicion of hypothyroidism. Diagnosis is based on reduced free T4 in combination with elevated TSH. Therapy using levothyroxine in the usual dose of 10 µg/kg BID does result in improvement in many but not all patients.

3. Polyradiculoneuritis/Botulism

The hallmark of generalized peripheral nervous system lesions on the neurological examination are generalized reduced segmental spinal reflexes. This finding in a tetraparetic/tetraplegic patient clearly indicates a generalized peripheral nervous system lesion. However, not all segmental spinal reflexes in all four limbs have to be reduced to the same extent. Often, withdrawal reflexes are most severely affected, whereas muscle tendon reflexes or muscle reflexes might still be preserved. In addition to the deficits described so far, innervation of the esophagus may be affected leading to megaesophagus in some dogs. Therefore, in any patient with suspected generalized peripheral neuropathy, taking chest radiographs is indicated.

Botulism

Botulism is a sometimes fatal disease characterized by muscular paralysis. It develops after ingestion of preformed botulinum toxin produced by the anaerobic bacterium Clostridium botulinum (less commonly Clostridium baratii, Clostridium butyricum). Toxins produced have different antigenic properties allowing differentiating between 7 different subtypes (A-F). In human beings, botulism is mainly caused by serotypes A, B, E whereas in dogs it is caused by serotype C and rarely type D. In dogs, botulism may develop following ingestion of carcasses or inadequately stored food or by drinking from contaminated ponds. The toxin is absorbed from the small intestine by endocytosis. It enters the lymphatic systems and it is distributed via blood stream. It binds rapidly and irreversibly to the neuronal surface of the pre-synaptical terminal of the neuromuscular junction. After being internalized it modifies the SNARE-protein which is responsible for acetylcholine release at the neuromuscular endplate. The impairment of acetylcholine release causes the typical flaccid paralysis. Botulism is characterized by a rapidly progressing paralysis, often starting in the rear limbs.

The more rapidly the symptoms develop, the more severe the disease tends to be. Clinical signs may occur within hours to several days following ingestion of toxin. Clinical signs reflect a progressive, symmetrical disorder, ranging from mild weakness to severe flaccid tetraplegia with absent segmental spinal reflexes. Those signs may be accompanied by weakness in muscles of the face, jaw, pharynx, and esophagus resulting in dysphonia, dysphagia, facial paralysis and megaesophagus. Mydriasis may be present. Pain perception remains normal and there is no evidence of hyperesthesia. Muscle atrophy is not seen. In severe cases, respiratory musculature might be affected resulting in a predominately diaphragmatic respiration. Sometimes, signs of autonomic dysfunction (mainly parasympathetic), such as changes in heart rate, mydriasis, keratoconjunctivitis sicca, urinary retention and constipation, can be seen. History and clinical symptoms are often suggestive of botulism.

Definitive diagnosis is based on toxin detection early in the disease (i.e., within 24 h) in blood, feces or gastrointestinal tract contents. Often a mouse biological assay is used for toxin detection. Due to the nature of the test, it may take several weeks to obtain a result. Alternatively, ELISA and PCR can be used but those are not widely available yet in veterinary medicine. Electrodiagnostic tests can be used to support a tentative diagnosis. Therapy is mainly supportive: soft bedding, urinary catheter, avoiding pressure sores and assisted feeding. Antitoxin application is discussed controversially. It will bind circulating toxin and therefore should be given early in the disease. The available trivalent antitoxin, however, acts against subtypes A, B and E. There is no commercially available antitoxin against the C, the one causing botulism in dogs. The prognosis is usually favourable in dogs, with recovery occurring within 1 to 3 weeks, although some affected dogs are euthanized due to other clinical complications or respiratory failure. Therefore, careful monitoring for signs of respiratory insufficiency is indicated.

Idiopathic Polyradiculoneuritis

Polyradiculoneuritis, generalized inflammation of nerve roots, may actually be a group of various etiopathologically different diseases. In the context of this presentation, we will focus on idiopathic polyradiculoneuritis. It is a suspected immune-mediated disease, most likely triggered by different stimuli, one of those presumably being raccoon saliva. Lesions involving nerve roots (more obvious in ventral than in dorsal roots) and the most proximal part of peripheral nerves are composed of segmental demyelination and mononuclear interstitial infiltration. The disease affects dogs of any breed, both sexes, and usually of adult age. Onset is marked by weakness and pelvic limb hyporeflexia, although thoracic limb involvement may sometimes be the initial and dominant clinical sign. Paralysis progresses rapidly, resulting in a flaccid symmetric tetraplegia. The duration of paralysis varies from several weeks to 2 or 3 months. Motor impairment is more pronounced than sensory changes, although many dogs appear to be hyperesthetic to sensory stimuli. Bladder and rectal paralysis are not usually observed. In severely affected animals, there may be complete absence of spinal reflexes, facial weakness, loss of voice, inability to lift the head and labored respiration. Megaesophagus seems to be much less common than in botulism. Respiratory insufficiency may be seen if phrenic nerves and/or intercostal nerves are affected as well. Electromyographic changes are more pronounced than those seen in botulism. There is extensive spontaneous muscle activity within 5 to 7 days after the onset of clinical signs. Motor nerve conduction velocity may be markedly reduced and M-wave temporal dispersion can be seen in many dogs. F-waves can be altered (e.g., prolonged F-wave latencies and F-wave dispersion, decreased F-wave amplitudes, increased F-wave ratio), depending on clinical signs and duration of disease reflecting that the primary pathology is located in nerve roots. Therapy is mainly supportive, similar as in botulism. Glucocorticosteroids do not seem to alter course of the disease. Patients with obvious hyperesthesia may benefit from specific medication for neurogenic pain: gabapentin: 5–10 mg/TID or pregabalin: 2–4 mg/kg BID. Intravenous application of human immunoglobulins (0.5 g/kg once or 0.5 g/kg on 3 consecutive days) can hasten recovery but may be cost prohibitive in most dogs. Prognosis is usually favorable, but dogs with severe axonal degeneration may die from respiratory paralysis or may have protracted, incomplete recoveries. Some animals may not show any clinical improvement. The overall course of the disease may be 4–6 weeks; however, recovery may take up to 6 months. Relapses are possible but rare.

4. Trigeminal Neuritis

Trigeminal lesions cause obvious neurological deficits if both mandibular branches carrying motor fibres are affected, whereas unilateral lesions or purely sensory deficits are often overlooked. Presenting complaints in bilateral trigeminal nerve motor deficits include inability to swallow, spilling of food and water around the feeding bowl, as well as excessive drooling. The inability to close the mouth is rarely recognised by the owner. However, dogs with trigeminal nerve dysfunction have a normal gag reflex. The inability to swallow is caused by the inability to close the mouth, which is the initial step of the swallowing process. Once the lower jaw is manually supported, the swallowing can be performed by affected dogs.

The complete neurological examination may reveal the following deficits in dogs with trigeminal nerve dysfunction:

1.  Motor deficits: inability to close the jaw, decreased resistance if the jaw is opened by the examiner.

2.  Sensory deficits: absent palpebral reflex, absent corneal reflex, absent lip retraction, absent nasal sensation.

About one third of dogs with motor deficits have sensory deficits as well. The majority of dogs with trigeminal neuropathy suffer from idiopathic trigeminal neuropathy (ITN). Much less common reasons are lymphosarcoma, neosporosis and polyneuritis. In dogs with ITN, trigeminal nerve deficits may sometimes be accompanied by additional facial nerve deficits and Horner's syndrome. Therapy of ITN consists of applying a flexible bandage to the mouth for feeding and drinking. Clinical signs usually resolve within 1–3 weeks.