Page 818 - Clinical Small Animal Internal Medicine

786 Section 8 Neurologic Disease

initially develops, ICP typically remains constant due to exquisitely sensitive for the detection of acute hemor-
VetBooks.ir a system of compensation known as cerebrovascular rhage in hemorrhagic stroke. Acute hemorrhage is evi-
dent as a hyperdensity on CT due to hyperattenuation
autoregulation. However, with progressive expansion of
the hematoma, these mechanisms become exhausted,
the first eight days following onset. The attenuation
after which further increases in the volume of the clot of X‐rays by the globin portion of blood, particularly for
become associated with a dramatic increase in ICP. decreases until the hematoma is isodense about one
In severe cases, this increase in ICP causes a decrease in month after the event. The periphery of the hematoma
perfusion of the brain and ultimately fatal herniation of contrast enhances from six days to six weeks after onset,
the brain at the level of the foramen magnum. due to revascularization.
Magnetic resonance imaging can be used to identify
Clinical Presentation ischemic stroke within 12–24 hours of onset and to
Neurologic signs seen in stroke patients are characteris- distinguish hemorrhagic lesions from infarction. T2‐
tically peracute or acute in onset and nonprogressive or weighted and FLAIR images are particularly useful in
regressive in their evolution. Initially, deficits observed imaging of ischemic stroke since they allow correlation
are usually focal, often asymmetric and ultimately related of the lesion with anatomic structures and vascular
to the area of the brain involved. The combination of territories. With these sequences, ischemic infarction
abrupt onset and focal, often asymmetric localization appears as a hyperintense lesion. The conformity of an
should raise the index of suspicion for vascular disease. infarct to a vascular territory is an important element in
The initial signs are then followed by an arrest and the diagnosis that helps in distinguishing these lesions
regression of the neurologic deficits in all except the fatal from other differentials. Ischemic infarcts are limited
strokes, although worsening of edema (associated with to the region of the brain vascularized by the affected
the secondary injury phenomena) can result in progres- vessel, and are often wedge‐shaped in appearance with
sion of neurologic signs for a short period of 24–72 resultant sharply demarcated borders. There is minimal
hours. In addition, intracranial hemorrhage can present to no mass effect associated with these lesions. Changes
with progression of signs for up to 24–72 hours before are best appreciated in the gray matter and are well visu-
regression as a result of reorganization of the hemor- alized in deep gray matter structures such as the thala-
rhage and edema resorption. mus and basal ganglia due to their selective vulnerability
Neurologic deficits usually reflect a focal anatomic to ischemia. Contrast enhancement (associated with
diagnosis and depend on the location of the vascular reperfusion) is not usually seen until at least 7–10 days
insult (telencephalon, thalamus, midbrain, pons, medulla, but the inverse is a useful indicator – lack of contrast
cerebellum). Infarction of an individual brain region is uptake in the ischemic region often results in a noticea-
associated with specific clinical signs that reflect the loss bly darker area on postcontrast T1‐weighted scans.
of function of that specific region. In the case of hemorrhagic stroke, particular character-
istics of hematoma evolution are useful in making the
Diagnosis diagnosis with conventional sequences. As the hematoma
Advanced imaging (CT, conventional and/or functional ages, oxyhemoglobin sequentially breaks down into sev-
MRI) is a prerequisite for confirming a diagnosis of eral paramagnetic products – first deoxyhemoglobin, fol-
stroke, for defining both the vascular territory involved lowed by methemoglobin, and finally hemosiderin. The
and the extent of the lesion, as well as distinguishing earliest possible detection of hemorrhage depends on the
between ischemic and hemorrhagic disease. Imaging conversion of oxyhemoglobin to deoxyhemoglobin which
studies are also necessary to rule out other causes of occurs after 12–24 hours. Whilst oxyhemoglobin pro-
neurologic deficit such as tumor, head trauma, and vides a signal similar to that of normal brain parenchyma,
encephalitis. the iron exposed to surrounding water molecules in the
Computed tomography images are frequently normal form of deoxyhemoglobin creates a signal loss, making it
during the acute phase of ischemic stroke, making the easy to identify on T2‐weighted and susceptibility‐
diagnosis of ischemic stroke using CT an exercise in the weighted sequences. Gradient echo (T2‐weighted)
exclusion of other differential diagnoses. In part, this is sequences are exquisitely sensitive to the disruption of
due to the relatively noisy CT images of the brain in the local magnetic field that this creates and show hemor-
animals with a large skull to brain ratio, compared with rhage as dense hypointense regions.
people. Early CT signs of ischemia can be subtle and In addition to conventional MRI sequences, several
difficult to detect even by very experienced readers and functional MRI (fMRI) techniques have been developed
include parenchymal hypodensity, loss of gray–white for the early diagnosis of stroke. These include diffusion
matter differentiation, subtle effacement of the cortical and perfusion imaging and magnetic resonance angiog-
sulci, and local mass effect. By way of contrast, CT is raphy (MRA). Diffusion‐weighted imaging (DWI) is