Clinical signs: The clinical signs reflect the side of the haemorrhage and are acute in onset. They can be multifocal.
Pathogenesis: Bleeding disorders can be inherited (e.g. von Willebrand’s disease) or acquired secondary to rodenticide toxicity or infectious / inflammatory diseases (e.g. immune-mediated thrombocytopenia, disseminated intravascular coagulation). Indeed, tick-borne infectious causes of vasculitis and thrombocytopenia, such as Rocky Mountain spotted fever, are common in some parts of the world. Haemorrhage into the CNS can occur with any bleeding disorder and, although unusual, it can be the first manifestation of the disease. For example, epidural haemorrhage causing spinal cord compression has been reported in Dobermann Pinschers with von Willebrand’s disease (). The presence of petechiae, ecchymoses or prolonged bleeding following venipuncture should alert the veterinarian to the possibility of a bleeding disorder. It is not unusual to find extensive extradural haemorrhage at the site of acute intervertebral disc herniations or vertebral fractures and luxations. These animals do not have an underlying coagulopathy; the haemorrhage has occurred as a direct result of disruption of the venous sinuses that overlie the disc.
Diagnosis: The history and clinical findings may be suggestive of a bleeding disorder. A buccal mucosal bleeding time can be performed to evaluate platelet function by gently tying the upper lip back with gauze to expose the mucosa, and then making parallel cuts 1 mm deep and 5 mm long with a blade and noting the time taken for bleeding to stop. Devices specifically designed to make these cuts are available commercially. Blood can be carefully blotted away as it runs down the gum, but the incision should not be touched. Bleeding times > 4.5 minutes are abnormal but there is a lot of individual variation (). If rodenticide toxicity is suspected, activated clotting time (ACT) should be measured. Values >120 seconds are supportive of a coagulopathy. Further evaluation of clotting function includes a manual platelet count, one-stage prothrombin time (OSPT) and activated partial thromboplastin time (APTT). The levels of individual clotting factors can be measured by specialist laboratories.
If a bleeding disorder is not suspected, a routine work-up for focal spinal cord signs should be undertaken. Survey radiographs are unremarkable, and cerebrospinal fluid may be diffusely haemorrhagic if the haemorrhage is intraparenchymal. If haemorrhage is extradural, it will be visible as a large mass on myelography and is readily identifiable on CT images if it occurred in the preceding 24 hours. MRI will detect both recent and old haemorrhages but the appearance changes with time (). If a haemorrhage is suspected based on imaging, surgery should not be undertaken unless the coagulation profile is normal.
Treatment and prognosis: Treatment is specific to the cause. For example, rodenticide toxicity can be treated with vitamin K1 (2.5-5 mg / kg s.c, then 0.25-5mg / kg orally, divided q8-12h for 5 days to 5 weeks, depending on the product involved) and a plasma or whole-blood transfusion if the patient is actively bleeding. Prognosis depends on the underlying aetiology and the severity of neurological dysfunction caused.
Clinical signs: Fibrocartilaginous embolism (FCE) causes peracute onset of non-painful neurological deficits, most commonly in the lumbosacral intumescence () but also in the brachial intumescence. Affected dogs are usually young and of large non-chondrodystrophoid breeds, engaged in exercise at onset of signs, but smaller breeds such as Shetland Sheepdogs, Miniature Schnauzers and Yorkshire Terriers can be affected and are more likely to have signs localizing to the sixth cervical to second thoracic spinal cord segments. Signs are often dramatically lateralized, producing hemiparesis. Involvement of the sympathetic tracts in the cervical spinal cord can result in Homer’s syndrome and vasodilation on the affected side. The vasodilation produces differential hyperthermia that can be detected by comparing the temperature in the front feet and comparing the external pinnae (which will be flushed on the affected side) (). FCE rarely occurs in cats but there is one report of a cervical FCE ().
Pathogenesis: FCE is a syndrome in which fibro-cartilage identical to that found in the nucleus pulposus embolizes to the spinal cord vasculature, producing an area of ischaemic necrosis centred on the spinal cord grey matter (). Signs are often lateralized, as the embolus usually lodges in one branch of the ventral spinal artery.
Diagnosis: FCE should be suspected in animals presenting with peracute onset of lateralizing signs in the absence of spinal pain. Cervical disc herniations as a result of trauma can produce a similar syndrome, with dramatic lateralization of signs and differential hyperthermia, but these animals usually have neck pain. Survey spinal radiographs are unremarkable and there is no evidence of spinal cord compression on myelography, though occasionally focal swelling of the cord is detected (). The infarcted area is visible on MR images. cerebrospinal fluid analysis may reveal disproportionately elevated protein and a neutrophilic pleocytosis.
Treatment and prognosis: Treatment centres around successful rehabilitation of the animal (). Improvement can be dramatic over the first 7 days and will continue for 1-3 months after injury.
The extent of recovery will depend on the extent of injury. If deep pain perception is preserved in the thoracic and pelvic limbs on the affected side, the prognosis is good. If deep pain perception is absent in one or more limbs, the prognosis is more guarded, but deep pain perception should be monitored weekly: its reappearance indicates the potential for recovery. The author has seen dogs that did not regain deep pain perception or use of the thoracic limb on the affected side, but recovered full use of their other three legs and were able to walk without problem.
Miscellaneous vascular diseases
Focal spinal cord deficits can be caused by emboli as a result of extreme hyperlipaemia (inherited in Miniature Schnauzers or associated with hypothyroidism), vegetative valvular disease (e.g. secondary to endocarditis) and neoplasia. A variety of different focal neurological deficits have been reported with extreme polycythaemia and leukaemia as a result of sludging of blood vessels.
Lower motor neuron disease
Lower motor neuron diseases that can cause tetraparesis are listed in Lower motor neuron diseases that can cause tetraparesis.
Lower motor neuron diseases that can cause tetraparesis.
|Mechanism of disease||Specific diseases|
|Degenerative||Inherited peripheral neuropathies: motor sensorimotor, sensory, metabolic |
|Inherited myopathies |
|Inherited junctional disease |
|Metabolic||Diabetes mellitus |
|Metabolic myopathies |
|Neoplastic||Paraneoplastic – insulinoma, other |
|Idiopathic||Distal denervating disease |
|Inflammatory||Chronic inflammatory demyelinating polyneuropathy |
|Myasthenia gravis |
|Polyradiculoneuritis: infectious (protozoal); immune-mediated |
|Polymyositis: infectious; immune-mediated |
|Tick paralysis |