Progressive Myelopathy Due to a Spontaneous Intramedullary Hematoma in a Dog: Pre- and Postoperative Clinical and Magnetic Resonance Imaging Follow-up
A 4-year-old, male Jack Russell terrier was presented for a 6-month history of progressive right hemiparesis with episodic cervical hyperesthesia. The neurological examination showed a right-sided, upper motoneuron syndrome and partial Horner’s syndrome. Two magnetic resonance imaging (MRI) examinations were performed 3 months apart and revealed a persistent cervical intramedullary hematoma. A dorsal myelotomy was performed. A subacute hematoma was confirmed histologically without underlying lesions. Eighteen months later, the dog’s clinical signs were minimal. Two MRI examinations were performed 2 weeks and 5 months after surgery and revealed regressing signal abnormalities at the surgical site, consistent with a surgical scar.
Introduction
Intramedullary bleedings are rare findings in veterinary medicine. However, with the increased availability of magnetic resonance imaging (MRI), antemortem hematomyelia has been described in veterinary medicine over the last few years.1–4 Most cases have been secondary to spinal cord trauma, especially disk herniation or Angiostrongylus vasorum infection or Leishmania infantum infection.1–4 In a meta-analysis of 613 human patients with spinal hematoma, only five intramedullary hematomas were observed.5 Most intramedullary bleedings described in human medicine literature were a result of tumors, syringomyelia, vascular malformations, and anticoagulant therapy or hereditary coagulopathies such as hemophilia and von Willebrand’s factor deficiency.6–13 Rarely, no evidence of precipitating factors or underlying lesions were found. Spontaneous hematomyelia secondary to cryptic vascular malformation or idiopathic spontaneous hematoma are then considered.9,14 Four types of vascular malformations can be involved in the pathogenesis of spontaneous hematomyelia—all of which are located in the parenchyma or in the subpial space.15–17
Capillary telangiectasia is a small collection of dilated capillaries of various diameters that are lined with endothelial cells and separated from one another by normal spinal parenchyma. In the spine, they often are located in the subpial space.15–17
Cavernous angiomas (also called cavernous venous malformations) are solitary, circumscribed, pinkish or dark-red masses representing honey-combed, small vascular channels that are lined by a single, thin endothelial layer separated by fibrous strands or septae. Intramedullary cavernous malformations are rare.15–17
Arteriovenous malformations, the most common type of congenital vascular anomalies in the spinal cord, are characterized by direct arterial venous communication without an intervening capillary bed. Dilated veins and arteries are often observed.15–18
Venous angiomas are congenital malformations composed exclusively of a group of abnormal veins separated by a normal neural parenchyma. These appear to be very rare in the spinal parenchyma.15–17
The veterinary literature has described four vascular malformations responsible for spontaneous hematomyelia in dogs: two arteriovenous malformations, one cavernous angioma, and one microangioma.19–22 In three dogs, the diagnosis was established postmortem; the microangioma was suspected after myelography and histological examination.19–22
This report describes the clinical evolution and the MRI before and after surgical treatment for a dog with progressive cervical myelopathy secondary to a histologically confirmed hematoma.
Case Report
A 4-year-old, male Jack Russell terrier was referred for right hemiparesis progressing for 6 months. The dog was current on vaccinations against rabies, canine distemper, Rubarth’s hepatitis, and parvovirus. The dog was presented with weakness in the right forelimb, which gradually increased in severity. A 1-month history of increasingly frequent falls and weakness in the right hind limb was also noticed. Fifteen days before consultation, the referring veterinarian observed conscious proprioceptive deficits and hypertonia in the right limbs. Four days before referral, the dog vocalized when moving his head from a permanent ventral flexion. This was interpreted as sharp cervical pain. Prednisone (0.7 mg/kg q 24 hours) (Cortancyla) was initiated, and a slight improvement was noticed.
During consultation, the owners reported an increased intake of water since the introduction of the corticotherapy, and the general examination was normal. The neurological examination revealed a normal mental status. The dog’s head was slightly turned toward the right. The right fore-and hind limbs demonstrated increased extensor tone and normal muscle volume. Intermittent, nonweight-bearing lameness and knuckling were observed on the right forelimb with wearing of claws. Ataxia and mild paresis affected the right limbs. Proprioceptive deficits were noticed in the right limbs, with more severity in the forelimb. The right forelimb withdrawal reflex was reduced in amplitude, possibly as a consequence of the increased extensor tone. Other spinal reflexes were of normal amplitude in all four limbs. A cervical hyperesthesia was demonstrated, especially during flexion on the right.
Myosis and dilated conjunctive vessels were observed on the right eye. The anisocoria increased in penumbra. Examination of the cranial nerves did not display other anomalies. Based on the clinical findings, the authors concluded the presence of an upper motoneuron syndrome on the right limbs with partial Horner’s syndrome on the right eye.
Complete blood count, coagulation profile, von Willebrand’s factor assay, and plain cervical radiographs were unremarkable. The dog was anesthetized for imaging and a cerebrospinal fluid (CSF) tap. A cervical computed tomography (CT) scanb was performed, and 1-mm contiguous axial sections were acquired before and after injection of iodinated contrast medium (2 mL/kg) (Télébrix 35c). No lesions were observed.
An atlantooccipital CSF tap was performed and revealed an albumin cytological dissociation (total protein 0.39 g/L, reference range <0.25 g/L). The cervical spine was evaluated by MRI [Figures 1A–1D]. A 0.2 Tesla permanent magnetd was used to obtain T1- and T2-weighted spin-echo sagittal and transverse images, with the dog in dorsal recumbency and placed in a quadrature radiofrequency extremity coil. Sagittal (slice thickness 3 mm, gap 0.2 mm) and transverse T1-weighted images (slice thickness 4 mm, gap 0.4 mm) were obtained after intravenous (IV) administration of gadolinium-chelate contrast agent (0.1 mmol/kg) (Dotareme).
An intramedullary lesion with sharp contours was demonstrated at the level of the fourth cervical vertebra (C4). The spinal cord was moderately enlarged. The lesion appeared hyperintense on T1-weighted sequences, with a hypo- to isointense center surrounded by a hyperintense periphery on T2-weighted sequences. A thin, hypointense ring was observed on T1- and T2-weighted sequences. The intervertebral disk between the sixth and the seventh cervical vertebrae (C6–C7) was hypointense on T2-weighted images. After contrast media injection, no enhancement was observed in the lesion or elsewhere. The main clinical diagnosis was an intramedullary subacute hematoma, dating from 5 days to 3 weeks. Additional differentials included a lipoma, a melanoma, or an inflammatory granuloma. Improvement was noted, and conservative treatment consisting of corticotherapy (prednisone 1 mg/kg q 24 hours, then at a decreasing dose) was recommended. The right forelimb lameness was the only residual abnormality.
Three months later, the dog showed an acute cervical hyperesthesia, and no improvement occurred after administration of prednisone or tramadol (Topalgicf). The dog’s neck was continuously curved to the right, and it was severely hemiparetic on the right. Another MRI was prescribed [Figures 2A, 2B], which demonstrated a severe enlargement of the spinal cord. The core of the lesion was hyperintense on T1-weighted sequences and hypointense on T2-weighted sequences. The periphery of the lesion was hypointense on T1-weighted sequences and hyperintense on T2-weighted sequences. The size of the lesion was 1.6 cm in length, 0.8 cm in width, and 1.0 cm in height. The lesion was consistent with a subacute bleeding surrounded by an edematous/cystic lesion. Because of the recurrence of bleeding and the failure of the medical treatment, surgical drainage of the hematoma was decided.
The dog was premedicated with midazolam (0.4 mg/kg IV) (Hypnovelg). Anesthesia was induced by an IV injection of propofol (4 mg/kg) (Rapinoveth) and maintained by isoflurane (Forènei) delivered in oxygen. Positive-pressure ventilation was initiated. The dog was maintained in ventral recumbency with light flexion of the neck. A dorsal median approach allowed exposure of spinous and articular processes from the third cervical to fifth cervical vertebrae. A dorsal laminectomy of C4 was performed by pneumatic drilling, preserving the cranial and caudal articular facets. A discolored, bluish lesion was identified throughout the periosteum and dura mater. A durotomy was performed. A longitudinal, right paramedian myelotomy revealed a 1.6-cm, dark fluid-filled cavity. Delicate aspiration with a microsuction tip allowed the cavity to drain, and biopsies of the dorsal and ventral wall were subsequently carried out. The spinal cord was gently rinsed with saline, and the durotomy was left opened. A free, autologous fat graft was placed over the laminectomy area, and the surgical approach was closed.
Dexamethasone (0.2 mg/kg q 24 hours IV) (Dexadresonj) was prescribed for 2 weeks. Analgesics consisted of a fentanyl patch (5 μg/kg per hour) (Durogesick) and gabapentin (150 mg q 12 hours per os [PO]) (Neurontinl). Urine retention was treated with alfuzosin (0.05 mg/kg q 12 hours PO) (Xatralm) for 2 weeks. The histological examination confirmed the presence of a hematoma in the neural parenchyma. The dorsal wall biopsy examination showed a vascularized granulation tissue with mononuclear cells and fibrous tissue, which was adjacent to leptomeninges. The ventral wall biopsy examination showed large neurons separated by edema and mononuclear cells. Tumoral cells or vascular malformations were not observed. A cryptic vascular malformation or an idiopathic spontaneous hematoma was the final diagnosis.
After surgery, the dog had increased extensor tone, remained in lateral recumbency, and was in pain for 3 days. Pain perception was present. After 10 days of standard supportive care, the dog was able to urinate and walk for a short period of time. Two weeks after surgery, an MRI was performed. In the sagittal and axial planes, T2- and T1-weighted images were acquired, and T1-weighted images were repeated after contrast media injection [Figures 3A–3C]. A lesion that was hyperintense on T2-weighted sequences and iso/hypointense on T1-weighted sequences with mild contrast enhancement was observed in the spinal cord at the original site of the hematoma. These images may be a result of the surgical scar or from the lesion responsible for the initial bleedings.
The dog was discharged, and physiotherapy was performed for 3 months. Three months after surgery, increased extensor tone was still observed on the right side with a complete conscious proprioceptive deficit on the right forelimb. Magnetic resonance imaging was performed to evaluate the evolution of the lesion [Figures 4A–4C]. Compared to the first postoperative diagnostic imaging, the lesion was better delineated and was hyperintense on T2-weighted sequences and isointense without contrast enhancement on T1-weighted sequences; this was consistent with the surgical scar. One and a half years after surgery, the dog was presented with a mild increased extensor tone on the right side. No recurrences of cervical hyperesthesia or nervous deficit were seen.
Discussion
This is the first report describing the clinical course and the MRI evolution of a surgically treated intramedullary hematoma with no apparent etiology in a dog. Systemic causes of bleeding, such as thrombocytopenia and coagulopathy, were excluded based on normal clinical and biological coagulation times, normal activity of the von Willebrand’s factor, and absence of abnormal bleeding at the time of surgery. No epidural or subarachnoidal bleeding (more frequently associated with coagulopathies and thrombocytopenias) was demonstrated at the time of surgery or analysis of the CSF.23,24
The dog was presented with a hemiparesis that developed over 6 months; however, vascular diseases are generally acute and nonprogressive.4,6,14,22,25 A gradual clinical course was previously described in a dog that was presented with an arteriovenous malformation of the cervical spinal cord, which was considered responsible for repeated ischemias and hemorrhages. In human medical literature, a chronic clinical course has been described in the context of underlying vascular malformations and anticoagulant treatments.9,20,26 A chronic clinical course has also been observed in human patients with spinal cord hematomas of undefined origin.9–11 For example, at the time of intramedullary cavernous malformations, four clinical presentations have been described: (1) acute episodes resulting in stepwise neurological deterioration; (2) slow progression of neurological deterioration; (3) acute onset of neurological deficit with rapid decline; and (4) acute onset of mild neurological deficit.26,27 The present case is intermediate to the first and the second situation. At the beginning, the deficit gradually worsened; then episodes of recurring and increasingly intense cervical hyperesthesia accompanied by aggravation of the nervous deficits were noticed. Clinical improvement was observed between each episode, as has been described in human patients.27 In the present dog, prognosis was good after surgery; this is similar to human patients in whom clinical symptoms progress chronically.28
Acute pain is also a common feature of spontaneous hematomyelia in human medicine.9–11,27,29 Acute pain has also been observed previously in four canine cases.19–22 In the present case, acute pain might be related either to the meningeal involvement, as shown from the histological examination, or to the dorsal horn lesion, as demonstrated by MRI. Lesion of the dorsal horn, the most important relay center for transmitting sensory information to the brain, is often associated with pain as described in syringohydromyelia.30–32 Sympathetically mediated pain also has been evoked in syringomyelia and in spinal cord injuries without precise explanation.30 A sign of sympathetic dysfunction, in the authors’ case report, is Horner’s syndrome. In association with moderated hemiparesis, cervical pain, and persistence of nociception, Horner’s syndrome evokes an intramedullary lesion. Axons of the primary neurons of the ocular orthosympathetic system advance in the reticulospinal tract, which is located deeply within the white matter.33,34 This syndrome has been reported in two of the three other cases of canine intramedullary cervical hematomas, whereas it has not been reported in subdural or epidural hematomas in dogs.20,22
Magnetic resonance imaging is the imaging modality of choice for the diagnosis, the follow-up, and the etiological investigation of intramedullary hematomas. Hemorrhages in the brain or spinal cord are best differentiated from other neurological conditions by MRI, which is a sensitive method for detecting neural hemorrhage and estimating its chronicity [see Table].14,35 The characteristics of the signal from a hematoma relate to the particular magnetic properties of hemoglobin and its degradation products, as well as to the protein content of the lesion. The changes in these properties may assist with estimation of its chronicity, even with a low field magnet.36,37 The principal difference between high field and low field in the evolution of a hematoma is the earlier appearance of the hyperintensity on T1-weighted sequences and the lower capacity to detect the hypointensity on T2-weighted sequences with a low field magnet. The hyperintensity on T1-weighted sequences represents the biotransformation of the desoxyhemoglobin into the methemoglobin, whereas the hypointensity on T2-weighted sequences is related to the susceptibility gradient generated by intracellular desoxyhemoglobin and methemoglobin or hemosiderin.
The first MRI features of the lesion were hyperintense on T1-weighted images and hypo- to isointense on T2-weighted images in the middle and in the extreme periphery; the lesion was hyperintense on T1-weighted images and T2-weighted images in between, without contrast enhancement. The peripheral hypointensity on T2-weighted sequences is consistent with hemosiderin associated with late subacute bleeding. The hyperintensity of the lesion on T1- and T2-weighted sequences is consistent with extracellular methemoglobin. Finally, the presence of a central zone with a lower hyperintensity than the periphery on T2-weighted sequences is consistent with the presence of desoxyhemoglobin. This implies that the hematoma dates from a few days to a few weeks. A T2*-weighted sequence would have helped to characterize the susceptibility effect of blood products.
In the second diagnostic imaging, the lesion was larger, and its signal had evolved. Three zones were distinguished: (1) a very thin peripheral zone that was hyperintense on the T1-weighted sequences and hypointense on the T2-weighted sequences due to either intracellular methemoglobin or (less likely) ferritin; (2) a hypointense zone on the T1-weighted sequences that was hyperintense on the T2-weighted sequences, corresponding to the cystic cavity found during surgery; this zone was a cystic remnant of previous bleedings; (3) a hyperintense zone on T1-weighted sequences that was clearly hypointense on T2-weighted sequences, suggestive of intracellular methemoglobin, corresponding to the hematoma found during surgery. The histological examination demonstrated a few days-old hematoma that was associated with more chronic remodeling, such as fibrous tissue and vascular proliferation. The evolution of the size of the lesion and its signal supported the recurrence of the bleeding and the enlargement of the lesion. This was an important element for the surgical decision.
In addition to diagnosing the hematoma and evaluating the bleeding date, MRI was performed to identify the cause of the hematoma. Magnetic resonance imaging may assist with the diagnosis of four diseases that are likely to result in an intramedullary hematoma: a disk herniation, a syringomyelia, a tumor, or a vascular malformation. The abnormal signal of C6–C7 on T2-weighted sequences was noted from the initial examination. This could have indicated a traumatic or ischemic origin of the bleeding, such as disk herniation or fibrocartilaginous embolism, respectively. However, the recurrence of the bleeding did not support this hypothesis.
In the absence of a cavity at the first examination, the syringomyelia was easily excluded. The cavity diagnosed during the second diagnostic imaging was considered to be a consequence and not a cause of the hematoma. Areas of central nervous system necrosis or liquefaction do not heal by vascular proliferation and fibroplasia; therefore, a cyst or cavity remains.34
A tumoral origin of the bleeding was not probable when evaluating the preoperative MRI results. The majority of tumors (11 out of 12 in a human study) showed contrast enhancement in human medicine as well as in veterinary medicine.12,35,38,39 Moreover, the presence of blood within a tumor seems preferentially associated with ependymomas, which are generally contrast enhanced.13,40 Histological examination confirmed the absence of tumor. The contrast enhancement observed on MRI 15 days postsurgery was more difficult to interpret; at the time of the MRI, one possible interpretation was that the presence of a neoplastic lesion was masked by the frequent bleedings. The disappearance of this contrast enhancement is consistent with a scar that was seen with a previous contrast enhancement, as has already been described after the excision of an intramedullary tumor in a man.41
The last hypothesis investigated through MRI involved a vascular malformation. Vascular malformations may demonstrate several patterns. They can appear as contrast-enhanced lesions associated with the presence of blood, such as a cavernous angioma. For example, tortuous vessels, especially on T1-weighted images, and signal-void artefacts on T2-weighted images may be observed with arteriovenous malformation.11,42–44 However, cryptic vascular malformations might be responsible for those spontaneous hematomyelia for the following reasons:
-
Certain cryptic malformations are not visible with MRI, especially with a low field magnet as used in the present case.14,45
-
No selective angiographic study was performed.
-
The malformation might have been destroyed during the last bleeding, thus preventing its diagnosis during the histological examination.
Cryptic vascular malformations are further supported by the repeated bleedings observed before surgery; this is similar to the clinical course of cavernous angioma.11
Conclusion
In this case report, a recurrent intramedullary hematoma was diagnosed noninvasively by sequential MRI performed in a dog that was presented with progressive cervical myelopathy. Diagnosis was confirmed by surgery, which led to complete recovery. The cause of the hematoma was not determined in this dog but is consistent with a spontaneous hematoma without neoplastic lesion or predisposing hemostasis deficiency. The postoperative MRIs revealed a temporary enhancement of the spinal cord parenchyma.
Cortancyl; Sanofi Aventis France Laboratory, Paris, France 75000
Scanner Hispeed CT/e Plus; General Electric Medical Systems, Milwaukee, WI 53219
Télébrix 35; Guerbet Laboratory, Roissy-Charles de Gaulles, France 95943
Signa Profile; General Electric Medical Systems, Milwaukee, WI 53219
Dotarem; Guerbet Laboratory, Roissy-Charles de Gaulles, France 95943
Topalgic; Sanofi Aventis France Laboratory, Paris, France 75000
Hypnovel; Roche Laboratory, Neuilly-sur-Seine, France 92200
Rapinovet; Schering-Plough Veterinary Laboratory, Levallois-Perret, France 92300
Forène; Abbott France Laboratory, Rungis, France 94150
Dexadreson; Intervet Laboratory, Beaucouze, France 49071
Durogesic; Janssen-Cilag Laboratory, Issy-les-Moulineaux, France 92130
Neurontin; Pfizer Laboratory, Paris, France 75000
Xatral; Sanofi Aventis France Laboratory, Paris, France 75000
Acknowledgments
The authors thank Dr. Dan Rosenberg for his advice, Racquel Cooper for her careful reading, and Dr. Pauline Couturier, the referring veterinarian.
![Figures 1A–1D—. Magnetic resonance images (MRIs) of the cervical spine.
(A) Precontrast, T1-weighted, sagittal MRI (TR 340 ms; TE 18 ms).
(B) T2-weighted, sagittal MRI (TR 3700 ms; TE 90 ms). (C) Precontrast, T1-weighted, transverse MRI (TR 380 ms; TE 18 ms). (D) T2-weighted, transverse MRI (TR 4480 ms; TE 85 ms).
These images show a T1-hyperintense and a T2-hypointense intramedullary lesion (filled arrowhead) surrounded by a T1- and T2-hyperintense lesion (open arrowhead). These signal patterns evoke intra- and extracellular methemoglobin found in late subacute hematoma. Note the thin T1- and T2-hypointense lesion on the ventral aspect of the hematoma, probably due to hemosiderin (C and D [chevron]). The total lesion measured 9 × 7 × 12 mm3 (width, height, length).](/view/journals/aaha/44/5/268_fig_1a.jpeg)
![Figures 1A–1D—. Magnetic resonance images (MRIs) of the cervical spine.
(A) Precontrast, T1-weighted, sagittal MRI (TR 340 ms; TE 18 ms).
(B) T2-weighted, sagittal MRI (TR 3700 ms; TE 90 ms). (C) Precontrast, T1-weighted, transverse MRI (TR 380 ms; TE 18 ms). (D) T2-weighted, transverse MRI (TR 4480 ms; TE 85 ms).
These images show a T1-hyperintense and a T2-hypointense intramedullary lesion (filled arrowhead) surrounded by a T1- and T2-hyperintense lesion (open arrowhead). These signal patterns evoke intra- and extracellular methemoglobin found in late subacute hematoma. Note the thin T1- and T2-hypointense lesion on the ventral aspect of the hematoma, probably due to hemosiderin (C and D [chevron]). The total lesion measured 9 × 7 × 12 mm3 (width, height, length).](/view/journals/aaha/44/5/full-268_fig_1a.jpeg)
![Figures 1A–1D—. Magnetic resonance images (MRIs) of the cervical spine.
(A) Precontrast, T1-weighted, sagittal MRI (TR 340 ms; TE 18 ms).
(B) T2-weighted, sagittal MRI (TR 3700 ms; TE 90 ms). (C) Precontrast, T1-weighted, transverse MRI (TR 380 ms; TE 18 ms). (D) T2-weighted, transverse MRI (TR 4480 ms; TE 85 ms).
These images show a T1-hyperintense and a T2-hypointense intramedullary lesion (filled arrowhead) surrounded by a T1- and T2-hyperintense lesion (open arrowhead). These signal patterns evoke intra- and extracellular methemoglobin found in late subacute hematoma. Note the thin T1- and T2-hypointense lesion on the ventral aspect of the hematoma, probably due to hemosiderin (C and D [chevron]). The total lesion measured 9 × 7 × 12 mm3 (width, height, length).](/view/journals/aaha/44/5/inline-268_fig_1a.jpeg)
![Figures 1A–1D—. Magnetic resonance images (MRIs) of the cervical spine.
(A) Precontrast, T1-weighted, sagittal MRI (TR 340 ms; TE 18 ms).
(B) T2-weighted, sagittal MRI (TR 3700 ms; TE 90 ms). (C) Precontrast, T1-weighted, transverse MRI (TR 380 ms; TE 18 ms). (D) T2-weighted, transverse MRI (TR 4480 ms; TE 85 ms).
These images show a T1-hyperintense and a T2-hypointense intramedullary lesion (filled arrowhead) surrounded by a T1- and T2-hyperintense lesion (open arrowhead). These signal patterns evoke intra- and extracellular methemoglobin found in late subacute hematoma. Note the thin T1- and T2-hypointense lesion on the ventral aspect of the hematoma, probably due to hemosiderin (C and D [chevron]). The total lesion measured 9 × 7 × 12 mm3 (width, height, length).](/view/journals/aaha/44/5/268_fig_1b.jpeg)
![Figures 1A–1D—. Magnetic resonance images (MRIs) of the cervical spine.
(A) Precontrast, T1-weighted, sagittal MRI (TR 340 ms; TE 18 ms).
(B) T2-weighted, sagittal MRI (TR 3700 ms; TE 90 ms). (C) Precontrast, T1-weighted, transverse MRI (TR 380 ms; TE 18 ms). (D) T2-weighted, transverse MRI (TR 4480 ms; TE 85 ms).
These images show a T1-hyperintense and a T2-hypointense intramedullary lesion (filled arrowhead) surrounded by a T1- and T2-hyperintense lesion (open arrowhead). These signal patterns evoke intra- and extracellular methemoglobin found in late subacute hematoma. Note the thin T1- and T2-hypointense lesion on the ventral aspect of the hematoma, probably due to hemosiderin (C and D [chevron]). The total lesion measured 9 × 7 × 12 mm3 (width, height, length).](/view/journals/aaha/44/5/full-268_fig_1b.jpeg)
![Figures 1A–1D—. Magnetic resonance images (MRIs) of the cervical spine.
(A) Precontrast, T1-weighted, sagittal MRI (TR 340 ms; TE 18 ms).
(B) T2-weighted, sagittal MRI (TR 3700 ms; TE 90 ms). (C) Precontrast, T1-weighted, transverse MRI (TR 380 ms; TE 18 ms). (D) T2-weighted, transverse MRI (TR 4480 ms; TE 85 ms).
These images show a T1-hyperintense and a T2-hypointense intramedullary lesion (filled arrowhead) surrounded by a T1- and T2-hyperintense lesion (open arrowhead). These signal patterns evoke intra- and extracellular methemoglobin found in late subacute hematoma. Note the thin T1- and T2-hypointense lesion on the ventral aspect of the hematoma, probably due to hemosiderin (C and D [chevron]). The total lesion measured 9 × 7 × 12 mm3 (width, height, length).](/view/journals/aaha/44/5/inline-268_fig_1b.jpeg)
![Figures 1A–1D—. Magnetic resonance images (MRIs) of the cervical spine.
(A) Precontrast, T1-weighted, sagittal MRI (TR 340 ms; TE 18 ms).
(B) T2-weighted, sagittal MRI (TR 3700 ms; TE 90 ms). (C) Precontrast, T1-weighted, transverse MRI (TR 380 ms; TE 18 ms). (D) T2-weighted, transverse MRI (TR 4480 ms; TE 85 ms).
These images show a T1-hyperintense and a T2-hypointense intramedullary lesion (filled arrowhead) surrounded by a T1- and T2-hyperintense lesion (open arrowhead). These signal patterns evoke intra- and extracellular methemoglobin found in late subacute hematoma. Note the thin T1- and T2-hypointense lesion on the ventral aspect of the hematoma, probably due to hemosiderin (C and D [chevron]). The total lesion measured 9 × 7 × 12 mm3 (width, height, length).](/view/journals/aaha/44/5/268_fig_1c.jpeg)
![Figures 1A–1D—. Magnetic resonance images (MRIs) of the cervical spine.
(A) Precontrast, T1-weighted, sagittal MRI (TR 340 ms; TE 18 ms).
(B) T2-weighted, sagittal MRI (TR 3700 ms; TE 90 ms). (C) Precontrast, T1-weighted, transverse MRI (TR 380 ms; TE 18 ms). (D) T2-weighted, transverse MRI (TR 4480 ms; TE 85 ms).
These images show a T1-hyperintense and a T2-hypointense intramedullary lesion (filled arrowhead) surrounded by a T1- and T2-hyperintense lesion (open arrowhead). These signal patterns evoke intra- and extracellular methemoglobin found in late subacute hematoma. Note the thin T1- and T2-hypointense lesion on the ventral aspect of the hematoma, probably due to hemosiderin (C and D [chevron]). The total lesion measured 9 × 7 × 12 mm3 (width, height, length).](/view/journals/aaha/44/5/full-268_fig_1c.jpeg)
![Figures 1A–1D—. Magnetic resonance images (MRIs) of the cervical spine.
(A) Precontrast, T1-weighted, sagittal MRI (TR 340 ms; TE 18 ms).
(B) T2-weighted, sagittal MRI (TR 3700 ms; TE 90 ms). (C) Precontrast, T1-weighted, transverse MRI (TR 380 ms; TE 18 ms). (D) T2-weighted, transverse MRI (TR 4480 ms; TE 85 ms).
These images show a T1-hyperintense and a T2-hypointense intramedullary lesion (filled arrowhead) surrounded by a T1- and T2-hyperintense lesion (open arrowhead). These signal patterns evoke intra- and extracellular methemoglobin found in late subacute hematoma. Note the thin T1- and T2-hypointense lesion on the ventral aspect of the hematoma, probably due to hemosiderin (C and D [chevron]). The total lesion measured 9 × 7 × 12 mm3 (width, height, length).](/view/journals/aaha/44/5/inline-268_fig_1c.jpeg)
![Figures 1A–1D—. Magnetic resonance images (MRIs) of the cervical spine.
(A) Precontrast, T1-weighted, sagittal MRI (TR 340 ms; TE 18 ms).
(B) T2-weighted, sagittal MRI (TR 3700 ms; TE 90 ms). (C) Precontrast, T1-weighted, transverse MRI (TR 380 ms; TE 18 ms). (D) T2-weighted, transverse MRI (TR 4480 ms; TE 85 ms).
These images show a T1-hyperintense and a T2-hypointense intramedullary lesion (filled arrowhead) surrounded by a T1- and T2-hyperintense lesion (open arrowhead). These signal patterns evoke intra- and extracellular methemoglobin found in late subacute hematoma. Note the thin T1- and T2-hypointense lesion on the ventral aspect of the hematoma, probably due to hemosiderin (C and D [chevron]). The total lesion measured 9 × 7 × 12 mm3 (width, height, length).](/view/journals/aaha/44/5/268_fig_1d.jpeg)
![Figures 1A–1D—. Magnetic resonance images (MRIs) of the cervical spine.
(A) Precontrast, T1-weighted, sagittal MRI (TR 340 ms; TE 18 ms).
(B) T2-weighted, sagittal MRI (TR 3700 ms; TE 90 ms). (C) Precontrast, T1-weighted, transverse MRI (TR 380 ms; TE 18 ms). (D) T2-weighted, transverse MRI (TR 4480 ms; TE 85 ms).
These images show a T1-hyperintense and a T2-hypointense intramedullary lesion (filled arrowhead) surrounded by a T1- and T2-hyperintense lesion (open arrowhead). These signal patterns evoke intra- and extracellular methemoglobin found in late subacute hematoma. Note the thin T1- and T2-hypointense lesion on the ventral aspect of the hematoma, probably due to hemosiderin (C and D [chevron]). The total lesion measured 9 × 7 × 12 mm3 (width, height, length).](/view/journals/aaha/44/5/full-268_fig_1d.jpeg)
![Figures 1A–1D—. Magnetic resonance images (MRIs) of the cervical spine.
(A) Precontrast, T1-weighted, sagittal MRI (TR 340 ms; TE 18 ms).
(B) T2-weighted, sagittal MRI (TR 3700 ms; TE 90 ms). (C) Precontrast, T1-weighted, transverse MRI (TR 380 ms; TE 18 ms). (D) T2-weighted, transverse MRI (TR 4480 ms; TE 85 ms).
These images show a T1-hyperintense and a T2-hypointense intramedullary lesion (filled arrowhead) surrounded by a T1- and T2-hyperintense lesion (open arrowhead). These signal patterns evoke intra- and extracellular methemoglobin found in late subacute hematoma. Note the thin T1- and T2-hypointense lesion on the ventral aspect of the hematoma, probably due to hemosiderin (C and D [chevron]). The total lesion measured 9 × 7 × 12 mm3 (width, height, length).](/view/journals/aaha/44/5/inline-268_fig_1d.jpeg)
Citation: Journal of the American Animal Hospital Association 44, 5; 10.5326/0440266
Citation: Journal of the American Animal Hospital Association 44, 5; 10.5326/0440266
Citation: Journal of the American Animal Hospital Association 44, 5; 10.5326/0440266
Citation: Journal of the American Animal Hospital Association 44, 5; 10.5326/0440266
Magnetic resonance images (MRIs) of the cervical spine. (A) Precontrast, T1-weighted, sagittal MRI (TR 340 ms; TE 18 ms). (B) T2-weighted, sagittal MRI (TR 3700 ms; TE 90 ms). (C) Precontrast, T1-weighted, transverse MRI (TR 380 ms; TE 18 ms). (D) T2-weighted, transverse MRI (TR 4480 ms; TE 85 ms). These images show a T1-hyperintense and a T2-hypointense intramedullary lesion (filled arrowhead) surrounded by a T1- and T2-hyperintense lesion (open arrowhead). These signal patterns evoke intra- and extracellular methemoglobin found in late subacute hematoma. Note the thin T1- and T2-hypointense lesion on the ventral aspect of the hematoma, probably due to hemosiderin (C and D [chevron]). The total lesion measured 9 × 7 × 12 mm3 (width, height, length).
Magnetic resonance images (MRIs) of the cervical spine, 3 months after the first MRI was performed. (A) Precontrast, T1-weighted, sagittal MRI. (B) T2-weighted, sagittal MRI. These images show a T1-hyperintense and a T2-hypointense intramedullary lesion (intracellular methemoglobin) corresponding to the clot found during surgery (open arrowhead). The fact that the T2 signal is more hypointense than the signal on the previous images indicates that a more recent bleeding had occurred between the two examinations. The clot was surrounded by a T1-hypointense and T2-hyperintense lesion diagnosed as a fluid-filled cavity during surgery (filled arrowhead). These signal patterns are suggestive of intra- and extracellular methemoglobin found in late subacute hematoma. Note the thin T1-hyperintense and T2-hypointense ring around the cystic cavity (chevron). The ring is probably due to intracellular methemoglobin. The lesion has increased in size (10 × 8 × 16 mm3) compared to the size at the previous examination.
Magnetic resonance images (MRIs) of the cervical spine, 2 weeks after myelotomy. (A) Precontrast, T1-weighted, sagittal MRI. (B) T2-weighted, sagittal MRI. (C) Postcontrast, T1-weighted, sagittal MRI. These images show a T2-hyperintense lesion. On precontrast T1-weighted images, a mixed hyper- and isointense signal is seen. Moderate enhancement is observed after contrast medium injection (filled arrowhead), due to the surgical scar. The lesion measured 7 × 7 × 21 mm3.
Magnetic resonance images (MRIs) of the cervical spine, 5 months after myelotomy. (A) Precontrast, T1-weighted, sagittal MRI. (B) T2-weighted, sagittal MRI. (C) Postcontrast, T1-weighted, sagittal MRI. These images show a T1-isointense, T2-hyperintense lesion without contrast enhancement (filled arrowhead). The lesion is more delineated than on the previous examination, and it measured 6 × 4 × 20 mm3.
