Clinicopathologic and MRI Characteristics of Presumptive Hypertensive Encephalopathy in Two Cats and Two Dogs
Two dogs and two cats were evaluated for the acute-onset of abnormal mentation, recumbency, and blindness. All cases had systemic hypertension, ranging from 180 mm Hg to 260 mm Hg. MRI of the brain disclosed noncontrast-enhancing, ill-defined, T2-weighted (T2W) hyperintensities in the white matter of the cerebrum in the areas of the frontal, parietal, temporal, and occipital lobes. Lesions were also observed in the caudate nuclei and thalamus (n = 1 in each). Intracranial hemorrhage was observed in one animal. Diffusion-weighted imaging (DWI) was consistent with vasogenic edema in two animals. Retinal lesions were observed in three animals. Hypertension was secondary to renal disease in three animals. A primary underlying disorder was not identified in one animal. Normalization of blood pressure was achieved with amlodipine either alone or in combination with enalapril. In one cat, hypertension spontaneously resolved. In three cases, neurologic improvement occurred within 24–48 hr of normalization of blood pressure. The presumptive diagnosis of hypertensive encephalopathy was supported by the MRI findings and neurologic dysfunction coincident with systemic hypertension in which the neurologic dysfunction improved with treatment of hypertension. The prognosis appears good for the resolution of neurologic deficits with normalization of blood pressure in animals with hypertensive encephalopathy.
Introduction
Systemic hypertension is increasingly recognized in small animals.1 The pathologic effect of systemic hypertension on tissues is referred to as target organ damage. Target organ damage can result when systolic blood pressure measurements begin to reach 150–160 mm Hg.1 A variety of tissues can be affected including the kidneys, eyes, cardiovascular system, and the central nervous system (CNS). In people, hypertensive encephalopathy is well recognized.2,3 In addition to the observation of systemic hypertension coincident with CNS dysfunction, the best criterion for confirming the diagnosis is the resolution of clinical signs with appropriate antihypertensive therapy. The signs of hypertensive encephalopathy often are reversible with the resolution of neurologic signs occurring within hours to the first few days of initiating therapy.1 Given the reversibility of clinical signs and anatomic distribution of the pathology observed in the caudal portions of the cerebrum, hypertensive encephalopathy in humans is often referred to as posterior reversible encephalopathy.2,3 Although hypertension underlies the majority of humans with posterior reversible encephalopathy, 20–30% of affected individuals are normotensive at the time of diagnosis.2,4 In humans, the underlying cause of the encephalopathy includes toxemia of pregnancy (preeclampsia/eclampsia), posttransplantation (e.g., bone marrow, solid organ), immune suppression with cyclosporine and tacrolimus, autoimmune disease, and secondary to chemotherapy.2
Hypertensive encephalopathy has been previously reported in dogs5 and cats.6,7 Hypertensive encephalopathy in those species can be observed with an acute (> 30 mm Hg) or a sustained (> 180 mm Hg) elevation in systolic arterial blood pressure.1,8 The clinical signs reflect involvement of the prosencephalon and include seizures, altered mentation, and blindness.6,9,10 Additionally, signs may refer to dysfunction of the CNS structures of the caudal fossa and include altered mentation, vestibular or cerebellar ataxia, and abnormal nystagmus.6,9,10 In people, the MRI findings in hypertensive encephalopathy have been described.2 To date, investigation of the clinicopathologic effects of hypertensive encephalopathy in animals have been limited to the gross and histologic response of the brain to experimental induction of systemic hypertension.8 Although CNS dysfunction may occur after renal transplantation, the underlying etiology may be multifactorial.9 To date, the clinicopathologic features and MRI findings of spontaneously occurring hypertensive encephalopathy in animals have not been reported.
The purpose of the present report is to describe the clinicopathologic characteristics and MRI findings involving the brain of four client owned animals with naturally occurring systemic hypertension and presumptive hypertensive encephalopathy. Given the similarity in the clinicopathologic characteristics and MRI findings in the affected dogs and affected cats, the cases are presented together. However, despite similarities, the underlying etiologies and pathogenesis of the individual animals may differ.
Case Report
Case 1
A 9 yr old shih tzu presented with a 1-wk history of ataxia and altered mentation. One wk prior to presentation the dog was examined by the referring veterinarian for a draining tract ventral to the left eye (oculus sinister [OS]). Surgical exploration failed to disclose an etiology, and the dog was referred. On presentation, physical examination was normal with the exception of a grade IV/VI left apical systolic murmur and a healing incision ventral OS. Indirect fundoscopic examination was normal in both eyes (oculus uterque [OU]). Neurologically, the dog was laterally recumbent and stuporous. Postural reactions were absent in all limbs. Spinal reflexes were normal. Cranial nerve examination revealed an absent menace OS and decreased menace response in the right eye (oculus dexter [OD]). Pupil size and pupillary light reflex (PLR) were normal OU. Bilateral nasal hypalgesia was present. The neuroanatomic diagnosis was consistent with a prosencephalic lesion.
Case 2
A 7 yr old spayed female Siamese presented with decreased appetite and lethargy. The cat had a history of renal dysfunction and constipation. Physical examination was normal with the exception of a grade I/VI parasternal systolic murmur. Indirect fundoscopic examination revealed retinal detachments OU. With the exception of an absent menace response, dilated pupils, and decreased PLR OU, neurologic examination was normal. Within 6 hr of presentation, the cat experienced a rapidly progressive change in mentation from alert and responsive to recumbent and unresponsive. Based on the abnormal mentation, the neuroanatomic diagnosis was consistent with a lesion involving either the prosencephalon or the brain stem, resulting in dysfunction of the ascending reticular activating system. As the blindness and abnormal PLR and pupil size were present prior to the change in mentation, those signs were attributed to the retinal lesions.
Case 3
A 10 yr old spayed female wirehaired fox terrier presented for evaluation of lethargy and decreased vision on the left side and difficulty finding her food. Additionally, the dog was hypothyroid and had a history of polyuria and polydipsia. Physical examination was normal with the exception of a grade IV/VI left apical systolic heart murmur. Indirect fundoscopic examination was normal OU. On neurologic examination, the dog’s mental state was depressed. The dog displayed an intermittent vestibular ataxia without a head tilt or pathologic nystagmus. Postural reactions were delayed in all four limbs. Spinal reflexes were normal. Cranial nerve examination revealed an absent menace response OS with a normal menace response OD. Pupil size and PLR were normal OU. The neuroanatomic diagnosis was consistent with multifocal disease with lesions involving the right prosencephalon and either the central vestibular system or cerebellum.
Case 4
A 19 yr old spayed female domestic shorthair presented for evaluation of multiple seizure-like episodes and a 2-wk history of lethargy. The cat was positive for the feline immunodeficiency virus (FIV). Twenty-four hr prior to presentation, the cat began head pressing and appeared blind. At presentation, physical examination was normal with the exception of a grade III/VI right parasternal systolic heart murmur. Indirect fundoscopic examination revealed partial retinal detachment OU. On neurologic examination, the cat was stuporous, laterally recumbent with periods of opisthotonus and decerebrate posture. Postural reactions were absent in all four limbs. Spinal reflexes were normal. Cranial nerve examination revealed an absent menace response, mydriasis, and incomplete PLR OU. Neuroanatomic diagnosis was consistent with a lesion affecting the prosencephalon or brain stem resulting in dysfunction of the ascending reticular activating system. The blindness and abnormal PLR and pupil size were attributed to the retinal lesions; however, a prosencephalic lesion with secondary caudal tentorial herniation resulting in compression of the midbrain could not be excluded from consideration.
Diagnostics
All animals underwent similar diagnostic testing to identify an underlying cause of hypertension and an etiology for neurologic dysfunction (Table 1). At the time of neurologic dysfunction, all animals had systemic hypertension measured using Doppler ultrasonography. In all cases, measurements were repeated 2–3× over several minutes to verify a consistent measurement. Subjectively, measurements did not vary by > 10 mm Hg in all cases. The measurement recorded in the medical record was the one with the highest systolic value. Systolic blood pressures ranged from 180 mm Hg to 260 mm Hg in all four animals. Other diagnostic tests included a complete blood count, serum biochemical profile, urinalysis, radiographic imaging of the thorax, and abdominal ultrasonography. In both cats, measurement of thyroid hormone levels, serum antibody titers directed against Toxoplasma gondii and coronavirus, and serum latex cryptococcal antigen agglutination test were performed. Echocardiography was performed in three cases. Urine protein/creatinine ratio was measured in cases 1 and 3. In three animals, cerebrospinal fluid obtained from the cerebellomedullary cistern was analyzed.
AUS, abdominal ultrasound; ABXR, abdominal radiograph; ALB, albumin; ALKP, alkaline phosphatase; ALT, alanine aminotransferase; BUN, blood urea nitrogen; CSF, cerebrospinal fluid; DSH, domestic shorthair; ECHO, echocardiogram; FeLV, feline leukemia virus; FIV, feline immunodeficiency virus; FLAIR, fluid-attenuated inversion recovery; M, male; OD, oculus dexter; OS, oculus sinister; OU, oculus uterque; PLI, pancreatic lipase; PO, per os; SF, spayed female; T1W, T1-weighted; T2W, T2-weighted; T4, total thyroxine; TXR, thoracic radiograph; UPC, urine protein/creatinine ratio; USG, urine specific gravity.
MRI Findings
An MRI of the brain was performed in all animals. In cases 1–3, the MRI was performed with a 3.0 Tesla unita using an extremity coil. In case 4, the MRI was performed with a 1.0 Tesla unitb using a head coil. The following fast spin echo sequences were obtained in the transverse planes: T2-weighted (T2W), T2W fluid-attenuated inversion recovery (T2W FLAIR), T1-weighted (T1W), and T1W FLAIR. In cases 1–3, a T1W FLAIR sequence was performed, and in case 4, a T1W sequence were performed. Either T1W FLAIR (cases 1–3) or T1W (case 4) sequences were also obtained after the IV administration of a contrast agentc (.1 mmol/kg). Additionally, a T2* gradient-recalled echo sequence (T2*W) was performed (cases 1–3) in an attempt to identify blood products. Imaging parameters for cases 1–3 were similar. The imaging parameters for T2W images were: an echo time (TE) of 82–83 msec, a repetition time (TR) of 4,000 msec, an echo train length (ETL) of 24–27, and a matrix of 320 × 256. Imaging parameters for T2W FLAIR images were: a TE of 82–83 msec, a TR of 4,000 msec, an ETL of 24–27, an inversion time (TI) of 2,250 msec, and a matrix of 320 × 256. Imaging parameters for T1W FLAIR images were: a TE of 121–127 msec, a TR of 9,502 msec, an ETL of 2, a TI of 1,067 msec, and a matrix of 320 × 256. Imaging parameters for T2*W images were: a TE of 11 msec, a TR of 517–600 msec, an ETL of 2, and a matrix ranging from 384 × 222 to 448 × 224. For all sequences, slice thickness ranged from 2 mm to 3 mm with a slice gap ranging from .2 mm to .5 mm.
In case 4, imaging parameters for T2W images were: a TE of 117 msec, a TR of 3,366 msec, and an ETL of 16. Imaging parameters for T2W FLAIR images were: a TE of 161 msec, a TR of 10,004 msec, an ETL ranging from 16 to 27 msec, and a TI of 2,200 msec. Imaging parameters for T1W images were: a TE of 12 msec, a TR of 316 msec, and an ETL of 2. For all sequences, the matrix was 256 × 160 and the slice thickness was 2 mm with a 2.5 mm gap.
In two animals (cases 2 and 3), diffusion-weighted imaging (DWI) was performed using a 2-dimensional echoplanar imaging. In an attempt to reduce the artifact induced by the magnetic susceptibility of the air-tissue interface of the frontal sinuses, the DWI sequences were obtained in a dorsal plane. Imaging parameters for the DWI were: a TE of 90 msec, a TR of 6,000 msec, a slice thickness of 2.4 mm with a 2.9 mm gap, and a matrix of 128 × 128. Postacquisition, an apparent diffusion coefficient (ADC) map was created for each case in which DWI was performed.
In all animals, lesions were identified in the white matter of the cerebrum. The topography of the lesions has been presented in Table 1. Briefly, the lesions involved multiple areas of the cerebrum, including areas of the cerebral hemispheres in the regions of the frontal, parietal, temporal, and occipital lobes, as well as the caudate nucleus and thalamus (Figures 1–3). The lesions were distributed within white matter of the cerebral hemispheres in the areas of the frontal, parietal, and occipital lobes in cases 1, 2, and 4. In case 4, the lesion also involved the white matter in the area of the temporal lobe of the cerebrum. In case 3, lesions were observed only in the white matter in the area of the left parietal lobe of the cerebrum and within the right thalamus adjacent to the dorsal aspect of the third ventricle (Figure 3). Finally, lesions were also observed in the caudate nuclei in case 1 (Figure 1A, D). In comparison with normal white matter, the lesions were hyperintense on T2W, T2W FLAIR, and T2*W sequences and isointense to hypointense on T1W FLAIR and T1W sequences. In all cases, the demarcation between the gray and white matter of the cerebrum was well defined as the hyperintense lesions in the white matter were of sufficient difference in their intensity so as to provide contrast to the overlying gray matter, which made the lesions more conspicuous and their margins more easily discernible. This was most obvious on the T2W FLAIR images. Conversely, within the white matter, the demarcation between the white matter with normal signal intensity and the white matter that was hyperintense was ill defined as the signal intensity gradually decreased at the periphery of the lesions. Abnormal contrast enhancement was observed only in case 1 in which there was subtle, ill-defined, diffuse enhancement of the caudate nuclei (Figure 1D). In one animal (case 2), a single, well-defined focal hypointense (signal void) was observed on the T2*W sequence in the gray matter of the endomarginal gyrus adjacent to the longitudinal fissure (Figure 4). The lesion was also hypointense on T2W and T1W FLAIR images and did not enhance after administration of contrast. The focal hypointensity was consistent with extravascular blood products (i.e., a focal hemorrhage). On the DWI sequence, the lesions in the white matter were less conspicuous. On the DWI sequence, the lesions were isointense; however, the lesions appeared hyperintense on postacquisition ADC maps (Figure 5).
Citation: Journal of the American Animal Hospital Association 49, 6; 10.5326/JAAHA-MS-5942
Citation: Journal of the American Animal Hospital Association 49, 6; 10.5326/JAAHA-MS-5942
Citation: Journal of the American Animal Hospital Association 49, 6; 10.5326/JAAHA-MS-5942
Citation: Journal of the American Animal Hospital Association 49, 6; 10.5326/JAAHA-MS-5942
Citation: Journal of the American Animal Hospital Association 49, 6; 10.5326/JAAHA-MS-5942
Based on the topography and the selective involvement and of white matter of the cerebrum, with the exception of the caudate nucleus (case 1) and thalamus (case 3), the differential diagnoses consisted of extracranial etiologies, including metabolic disorders such as hypertensive encephalopathy, nutritional excesses or deficiencies, toxicity, or degenerative etiologies. Infrequently, lesions in cerebral white matter have been observed in hepatic encephalopathy.11,12 Toxins that affect the white of the cerebrum include hexachlorophene and bromethalin intoxication.13,14 In dogs, degenerative etiologies that affect the white matter can be considered leukodystrophies. Leukodystrophies have been reported in Dalmatians, Labrador retrievers, Scottish terriers, Bernese mountain dogs, and miniature poodles.15–20 Included in the leukodystrophies are the congenital hypomyelinating syndromes of the CNS and spongy degeneration of the white matter of the CNS. Spongy degeneration has been reported in several breeds of dog and Egyptian Maus.12,21–25
None of the animals in this report had clinicopathologic findings suggestive of hepatic disease or dysfunction. Moreover, an exposure to intoxicants had not been reported, and all animals were fed commercially prepared diets. Equally unlikely to underlie the MRI changes, the leukodystrophies are observed at a young age and in specific breeds. Consequently, a presumptive diagnosis of hypertensive encephalopathy was established in all cases. In case 4, a differential diagnosis of FIV encephalopathy was also considered. FIV can cause either an acute or chronic encephalopathy.26,27 The acute form of FIV encephalopathy is characterized by a mononuclear perivascular infiltrate within the meninges and choroid plexuses. Gliosis and the formation of glial nodules are also consistent findings.26,27 The chronic form of FIV encephalopathy is characterized by atrophy of the white matter and basal nuclei.26,27
Outcome
Systemic hypertension was attributed to protein-losing nephropathy and chronic renal failure in cases 1, 3, and 4. In case 2, an underlying cause for hypertension was not identified. With the exception of systemic hypertension, an alternate extracranial etiology for neurologic dysfunction was not identified in any cases. Similarly, a primary intracranial etiology other than the consequence of hypertension was not identified in any case. Based on the evidence of concurrent target organ damage (retinal detachment in three cases) and the clinical response to antihypertensives in all cases, a diagnosis of hypertensive encephalopathy was considered most likely. The resolution of neurologic dysfunction occurred concurrent with normalization of systemic blood pressure in all cases. In all cases, the neurologic signs improved within the first 24–48 hr. There was complete resolution of neurologic signs in all cases when the animals were re-examined 2 wk after hospital discharge. In all cases, systemic hypertension was treated with recommended dose of amlodipined either alone or in conjunction with enalaprile. Cases 1, 2, and 4 all received concurrent prednisonef therapy at a tapering dose. It was possible to eventually discontinue the prednisone within 2 wk in all three cases in which it was administered. Ultimately, all animals remained free of neurologic signs without corticosteroids for the duration of their follow-up periods.
Although hypertensive encephalopathy was presumed in all cases, it is possible that the systemic hypertension was secondary to an acute increase in intracranial pressure, referred to as the Cushing reflex. The Cushing reflex results from hypoxia/ischemia to certain brainstem structures leading to sympathetic activation. That sympathetic tone causes an increase in systemic blood pressure with a decrease in heart rate and respiratory rate. That is the proposed mechanism for maintaining normal cerebral perfusion pressure secondary to intracranial hypertension. Arguing against that theory, evidence of brain herniation suggestive of increased intracranial pressure was not observed on MRI in any case. Additionally, attenuation of the intracranial subarachnoid space, as can occur with diffuse brain swelling, without concomitant brain herniation was not observed in any animal, further refuting the possibility that systemic hypertension was secondary to increased intracranial pressure. Likewise, with the exclusion of systemic hypertension, an intracranial etiology was not identified based on MRI and cerebrospinal fluid analysis. Moreover, with the exception of corticosteroids, specific treatment directed at an intracranial pathology was not instituted. However, clinical improvement secondary to corticosteroid administration cannot be completely excluded despite the ability to withdraw the corticosteroids without recurrence of clinical signs.
Discussion
To the authors’ knowledge, this is the first report to document the clinicopathologic features and MRI characteristics of hyperintensive encephalopathy. The cases presented in this report share common clinicopathologic findings, including the presence of systemic hypertension coincident with neurologic deficits combined with the resolution of neurologic deficits with the normalization of the blood pressure. Although the neurologic deficits varied, the prosencephalon was implicated in all cases. Unique to this report, the MRI characteristics documented herein share features in common with lesions observed on MRI with hypertensive encephalopathy in humans. The most commonly affected region in this case series was the white matter within the parietal and occipital lobes. Moreover, the MRI characteristics of the lesions were consistent with vasogenic edema. In humans, hypertensive encephalopathy typically involves the white matter of the parietal and occipital lobes of the cerebrum, but involvement of the frontal lobe, basal nuclei, brainstem, and cerebellum may also be seen.2,4,28 Moreover, the distribution of predominant lesions allows classification into syndromes based on topography and includes four regions: holohemispheric watershed, superior frontal sulcus, dominant parietal/occipital, and partial/or asymmetric (i.e., partial, asymmetric, combination); however, more than one region of the brain often is observed.28 As in humans, lesions in the present cases were observed most often in the parietal and occipital lobes of the cerebrum. As in case 2, intracranial hemorrhage has been observed in humans with hypertensive encephalopathy.29,30
Although the pathogenesis of hypertensive encephalopathy is not completely understood, the most widely held explanation suggests that the lesions are likely the consequence of vasogenic and interstitial cerebral edema as a result of failed auto-regulation of the cerebral vasculature.3,8 When the myogenic auto-regulatory mechanisms for cerebral perfusion are compromised, hyperperfusion ensues. Hyperperfusion results in the alteration of the blood-brain barrier that leads to the development of vasogenic edema. An alternative explanation has been proposed in affected humans whereby the lesions may be the consequence of initial hypoperfusion secondary to a systemic inflammatory response and endothelial activation and injury.3 Secondarily, systemic vasoconstriction ensues to increase perfusion and reverse brain hypoxemia.3 Auto-regulatory vasoconstriction in response to initial hypoperfusion may further reduce brain perfusion and induce ischemia, leading to the development of edema.3
Consistent with the characteristics of the lesions identified on MRI in the present cases, vasogenic edema typically produces increased signal intensity within the white matter on T2W images.2,28 In further support, lesions related to vasogenic edema are hyperintense on both the DWI and ADC mapping, suggesting a T2 shine-through phenomenon related to unrestricted diffusion of protons (mobile protons) that occurs with vasogenic edema.31 In contrast, cytotoxic edema results in a hyperintensity on DWI and a hypointensity on an ADC map.31 Hyperintensity of the white matter of the cerebrum has been observed on DWI and ADC mapping in hyperintensity encephalopathy in humans.32 In the two cases reported here in which DWI was performed, a similar pattern was appreciated on the DWI and ADC maps. Although the lesions were isointense compared with the gray matter on DWI, they were also hyperintense on the ADC maps. The ADC maps were consistent with vasogenic edema; however, the DWI should typically have the same imaging characteristics for gray and white matter that is observed on the T2W images. Although speculative, it is possible that vasogenic edema increased the signal intensity on the DWI and altered the contrast resolution between the gray and white matter.
Vasogenic edema has a predilection for the white matter related to the relatively loose composition of the myelinated fibers in a matrix of glial cells, arterioles, and capillaries.8 The predilection for affecting the posterior regions of the cerebrum in humans may be explained by a difference in the sympathetic innervation of the cerebral vasculature in which the degree of sympathetic innervation decreases from anterior to posterior regions of the brain, with the least sympathetic innervations present at the basilar artery.4 As a result, the more sparsely innervated vascular beds of the posterior regions of the cerebrum may be more susceptible to the effects of hypertension.4
Ultimately, the diagnosis of hypertensive encephalopathy in the present cases remains presumptive. Support for hypertensive encephalopathy is provided by the MRI findings. This is the first report to document such lesion in dogs and cats with systemic hypertension. Furthermore, neurologic deficits were observed concurrent with systemic hypertension. Importantly, neurologic deficits resolved with normalization of systemic blood pressure. Additionally, other etiologies to account for the lesions observed on MRI were not identified. Based on the cases presented here, the prognosis for resolution of neurologic signs appears favorable with the control of systemic hypertension. The long-term outcome likely will be related to the underlying cause of systemic hypertension.
Conclusion
Hypertensive encephalopathy should be considered a differential diagnosis in animals with T2W hyperintensities affecting the white matter within the parietal and occipital lobes. The lesions may also be present within the caudate nuclei and brainstem. T2W hyperintensities affecting the white matter of the cerebrum should prompt measurement of systemic blood pressure. In hypertensive animals, antihypertensive therapy should be initiated to reverse target organ damage to the brain.
Transverse MRIs of the brain of a 9 yr old shih tzu reveal lesions involving the caudate nuclei and white matter of the cerebrum in the area of the parietal and occipital lobes. A: On T2-weighted fluid-attenuated inversion recovery (T2W FLAIR) images, ill-defined hyperintensities are observed in the caudate nuclei (arrows) and the white matter of the parietal lobe (arrowhead). B: Caudally, similar hyperintensities are observed in the area of the occipital lobes (arrows). C: At the same level as A, the caudate nuclei appear normal on T1-weighted (T1W) FLAIR images. D: At the same level as C, the caudate nuclei display enhancement after contrast administration on TW1 FLAIR images (arrows). There is also scant contrast enhancement within the centrum semiovale (arrowhead).
Transverse T2W FLAIR MRIs of the brain of a 7 yr old Siamese that experienced a rapid and severe decline in mental state. A: At the midcerebrum, there are ill-defined hyperintensities in the white matter of the cerebrum in the region of the parietal lobes (arrows). B: Caudal to the image A, similar lesions are observed in the white matter in the region of the occipital lobes (arrows).
Transverse T2W FLAIR MRIs of the brain of a 10 yr old wirehaired fox terrier that was evaluated for lethargy and left-sided blindness. There are ill-defined hyperintensities in the white matter of the internal capsule and centrum semiovale (arrows) extending into the corona radiata in the region of the parietal lobes of the cerebrum on the right.
A: In the T2* gradient-recalled echo sequence (T2*W) from the cat in Figure 3, there is either a small focal hypointensity or signal void (arrow) consistent with extravascular blood products (hemorrhage) that is evident in the right cerebrum adjacent to the longitudinal fissure. B: In the T2W image, the lesion is hypointense (arrow), albeit less conspicuous than on the T2*W image. The adjacent white matter is hyperintense (arrowhead). Inset: The lesion appears hypointense (arrow) in the T1W FLAIR image.
A: In the dorsal plane, a diffusion-weighted image (DWI) from the dog in Figure 2, the white and gray matter are isointense. B: A hyperintensity is observed in the apparent diffusion coefficient (ADC) map (arrow). Inset: The hyperintensity in the ADC map is in the area of the hyperintense region of the white matter of the cerebrum on the T2W images (arrow).
Contributor Notes
