Clinical signs: Dermoid sinuses more often occur in the cervical region but can involve the thoracolumbar region (). Neurological examination is normal in the non-communicating form but neurological signs may occur if the sinus communicates with the dura or becomes infected (). Neurological signs reflect the neuroanatomical localization of the sinus. Close inspection of the hair on the midline may reveal abnormal placement.
Pathogenesis: Dermoid sinus is an inherited neural tube defect in the Rhodesian Ridgeback () but has also been reported in other breeds (). The defect results from incomplete separation of the skin and neural tube during embryonic development (). The sinus often extends from the skin to the supraspinous ligament as a closed sac filled with keratin debris. Communication with the subarachnoid space can predispose to meningomyelitis.
Diagnosis: Diagnosis is based on physical examination; radiography can be used to evaluate the extent of the sinus. Contrast radiography, using a non-ionic contrast medium (e.g. iohexol), determines whether the tract is closed and non-communicating or open and communicating with the spinal canal. Myelography determines the amount of spinal cord displacement. MRI or CT may define other neural tube defects in a communicating dermoid sinus ().
Treatment and prognosis: The treatment requires surgical excision (). A laminectomy is ‘equired for complete dissection of the sinus from the involved dura.
The prognosis is excellent in patients that have no neurological signs and no associated communication oetween the sinus and the spinal cord. Residual neurological deficits may be present if the spinal cord is involved.
Clinical signs: Clinical signs are reflected as pain and loss of function during active bone growth. Progressive paraparesis is the most common neurological finding.
Pathogenesis: Osteochondromatosis, known also as multiple cartilaginous exostoses, has been described in young dogs, cats and horses (). Bony growths arise in any bone formed by endochondral ossification. Outgrowths are related to the metaphysis of growing bones. Lesions are present in the axial and appendicular skeleton. Vertebral involvement is common in dogs.
Diagnosis: The bony lesions are characterized radio-graphically as variably sized circumscribed radiopaque densities with radiolucent areas (). CT can aid in the characterization of osteochondromas (). Definitive diagnosis is made by histopathology.
Treatment and prognosis: The masses should be surgically excised if there is appendicular or neurological dysfunction ().
Prognosis is dependent on the severity of the neurological deficits at presentation. The exostoses usually stop growing after closure of the physes and so the surgical removal of the masses, if spinal cord compression is occurring, can result in a successful outcome, but prognosis is dependent on the severity of neurological signs at presentation.
Clinical signs: Vertebral anomalies are often minor and usually cause no clinical signs. Malformations involving the spinal cord are more likely to cause neurological deficits, the nature of which is determined by the location of the abnormality.
Pathogenesis: Vertebral anomalies are common in the ‘screw-tailed’ breeds of dog such as Bulldogs and Boston Terriers, and the ‘tail-less’ cat, the Manx (). Spinal cord and vertebral anomalies have been classified by Bailey (1975) into two major groups (Vertebral and spinal abnormalities of the spine) based on embryological origin:
Abnormalities originating in the tissues of mesodermal origin (vertebrae and intervertebral discs)
Abnormalities originating from the tissues of ectodermal origin (spinal cord and meninges).
Mesodermal anomalies involve failure of vertebral separation orfusion. Important diseases are described in. more detail below.
Vertebral and spinal abnormalities of the spine:
|Malformation||Type of abnormality||Clinical signs|
|Malformations of the vertebral body and intervertebral disc|
|Block vertebrae||Lack of segmentation of somites and fusion of adjacent vertebrae||Rarely of clinical significance; may cause spinal stenosis|
|Butterfly vertebrae||Sagittal cleft in the vertebral body due to presence of notochordal remnants||Incidental finding; common in brachycephalic, screw-tailed breeds|
|Hemivertebrae||Failure of ossification in part of the vertebral body and lack of vascularization||Scoliosis, lordosis and kyphosis; compressive myelopathy; instability|
|Transitional vertebrae||Vertebrae with characteristics of adjacent divisions of vertebral column||Usually not clinically significant; sacralization of the lumbar vertebrae has been associated with lumbosacral syndrome|
|Spinal stenosis||Can occur with congenital anomalies. The vertebral column is small due to reduced pedicle size or excessive facet size||May cause compressive myelopathy|
|Malformations of the spinal cord and meninges|
|Spina bifida occulta||Defect involving only incomplete closure of one or more vertebral arches||Usually an incidental radiographic finding|
|Spina bifida (manifesta, cystica or aperta)||A defect in the vertebral arch with protrusion of meninges with or without spinal cord structures||Manifesta: implies associated clinical signs
Cystica: implies meningocele or meningomyelocele
Aperta: lesion communicates with environment
|Meningocele||Herniation of meninges from the vertebral canal through the bony defect; spinal cord remains in canal|
|Meningomyelocele||The meningeal sac contains the spinal cord||Usually associated with severe neurological deficits; may be identified as a dorsal midline mass|
|Sacrocaudal dysgenesis||Defective or absent formation of sacral or spinal cord segments||Associated with severe neurological impairment (typically S1-S3)|
|Rachischisis||Vertebral canal opened the entire length; contents of spinal cord exposed||Often not compatible with life|
Diagnosis: The diagnosis is suspected based on clinical signs, age and breed. Diagnosis of vertebral anomalies is based on survey radiographic findings (). Myelography is useful for determining extent of compression, stenosis or other possible spinal cord deformities (). MRI is more sensitive for determining spinal cord involvement.
Treatment and prognosis: If clinical signs are non-progressive, conservative management is recommended. Decompressive surgery is recommended with clinical signs of compressive myelopathy. Likewise, spinal instability and malalignment require vertebral stabilization techniques.
The prognosis is good for most vertebral anomalies because the majority of cases do not produce clinical signs. The prognosis is considered guarded if signs of spinal cord dysfunction are present. Multiple anomalies may exist concurrently.
Parenchymal spinal cord malformations
Malformations involving the spinal cord parenchyma are often referred to as myelodysplasia. This term also refers to a number of abnormalities of embryological development including spinal dysraphism and syringomyelia (). Dysraphisms are congenital defects that result from the failure of the neural tube to close; however, no fusion defects have been documented. Conditions affecting the vertebral column and/or the spinal cord include spinal dysraphism, syringomyelia, spina bifida with or without meningomyelocele and caudal vertebral hypoplasia ().
Spinal dysraphism: Spinal dysraphism was first documented in the Weimaraner () but has been described in many other breeds including the Rottweiler (), Dalmatian (), Alaskan Malamute (), Chihuahua () and Golden Retriever ().
Clinical signs: Characteristic clinical signs include a hopping gait, crouched stance, wide-based stance and reduced postural reactions. Head tilt, tail abnormalities and scoliosis have also been recognized in some dogs. Scoliosis is a reflection of denervation muscle atrophy subsequent to damage to the grey matter and associated LMN signs. Signs are evident as early as 4-6 weeks of age. There is a poor correlation between severity of histopathological lesions and clinical signs. Clinical signs often remain static.
Pathogenesis: Spinal dysraphism is thought to be inherited in the Weimaraner as a co-dominant lethal gene (). Histopathology of the spinal cord reveals asymmetry of grey matter with neuronal ectopia and syringohydromyelia.
Diagnosis: Survey spinal radiography may reveal evidence of scoliosis. Syringomyelia is detected by MRI. Definitive diagnosis is based on histopathology ().
Treatment andprognosis:Tnere is no treatment for this disorder. As clinical signs often remain static the prognosis depends on the functional capabilities of the dog for its resultant quality of life.
Syringohydromyelia: Syringomyelia refers to a disease where a tubular cavitation filled with CSF extends Through many spinal cord segments (). Hydromyelia is characterized by accumulation of CSF within an enlarged central canal of the spinal cord. These diseases occur most commonly, but not exclusively, in the cervical spinal cord and are described in full in site.
Clinical signs: Neurological signs reflect the neuroanatomical localization of the stenosis. Onset is usually insidious and progressive.
Pathogenesis: Congenital spinal stenosis indicates a malformation of the spine present at birth and occurs as a primary lesion or in association with other anomalies that predispose to stenosis (). Relative stenosis refers to canal narrowing that does not cause compression of neural tissue; whereas, absolute stenosis refers to a stenosis causing spinal cord compression (). Doberman Pinschers have a relative stenosis that most commonly involves the cranial thoracic vertebrae (T3-T6) (). Spinal cord compression usually is not evident on myelography.
Diagnosis: A diagnosis is based on plain film radiography that defines associated vertebral anomalies but requires myelography to determine the presence of stenosis. MRI of the spinal cord is recommended to further delineate associated neural tissue anomalies or abnormalities ().
Treatment and prognosis: Surgical decompression may relieve the compression; however, associated vertebral and spinal cord anomalies need to be taken into account.
The prognosis is considered guarded due to chronicity and presence of other anomalies. The lack of information available with regard to surgical follow-up makes it difficult to give an accurate prognosis.