Second edition

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282 Other major syndromes
antidepressants can prevent the appearance of depression.
In this regard, both nortriptyline and fluoxetine were found
effective; notably, however, when these medicines were discontinued
after approximately 2 years of continuous treatment,
whereas the fluoxetine-treated patients did well, the
nortriptyline-treated patients were more likely to subsequently
develop a depression (Narushima et a. 2002).
Sertraline has also been studied, with one study (Rasmussen
et al. 2003) demonstrating prophylactic efficacy and another
not (Almeida et al. 2006).
Anxiety
Chronic anxiety is seen in a small minority of stroke
patients and appears to be more common with right hemisphere
infarctions.
In most cases of anxiety seen after stroke, the anxiety,
rather than occurring in an isolated fashion, rather is part
of a post-stroke depression and in such cases an additional
diagnosis should not be made. Other differential possibilities
include alcohol or benzodiazepine withdrawal, and
general medical conditions such as chronic obstructive
pulmonary disease or hypocalcemia.
Benzodiazepines are often prescribed: caution should
be exercised here, however, as post-stroke patients may be
more likely to develop cognitive deficits or lethargy secondary
to these medications.
Other sequelae
Emotional incontinence, discussed further in Section 4.7, is
characterized by displays of uncontrollable laughter or crying
without any corresponding emotion and occurs secondary
to bilateral interruption of the corticobulbar tracts.
Nortriptyline (Robinson et al. 1993) and citalopram in doses
of 10–20 mg/day (Andersen et al. 1993) are both effective.
A catastrophic reaction, as discussed further in Section
4.24, may be seen in close to 20 percent of patients and
appears to be particularly common with infarction of the
anterior left hemisphere or the left basal ganglia.
The frontal lobe syndrome, discussed in Section 7.2,
may be seen with infarction or hemorrhage of the frontal
lobes, caudate nucleus, or thalamus. Patients may present
with varying combinations of disinhibition, perseveration,
and affective changes.
Mania is a rare sequela to stroke and, as discussed in
Section 6.3, may be seen after infarction of the midbrain,
thalamus, anterior limb of the internal capsule, and adjacent
head of the caudate nucleus, or the frontal or temporal lobes.
Psychosis, likewise, is a rare sequela, and, as discussed in
Section 7.1, may occur with infarction of the frontal or
temporal cortex, or the thalamus.
Etiology
The etiology of stroke varies according to whether it is due
to ischemic infarction, intracerebral hemorrhage, subarachnoid
hemorrhage, intraventricular hemorrhage, or cerebral
venous thrombosis, and each of these is discussed in turn.
Certain rare or unusual other causes of stroke, such as cerebral
autosomal dominant arteriopathy with subcortical
infarcts and leukoencephalopathy (CADASIL), are then
discussed, followed by a suggested work up for the new
stroke patient.
ISCHEMIC INFARCTION
Ischemic infarction occurs when arterial blood supply is
reduced below that required for tissue viability and such
reductions may occur via a variety of mechanisms. First,
embolic infarctions occur when an embolus, say from the
heart, lodges in an artery, thus occluding it. Second, thrombotic
infarctions occur when a thrombus forms inside an
artery, typically on top of an ulcerated atherosclerotic
plaque, causing occlusion. These two mechanisms account
for most large vessel syndromes, and may also underlie certain
of the lacunar syndromes. Third, low-flow (watershed)
infarctions occur secondary, not to occlusion, but to a critical
reduction in perfusion pressure. Fourth, and finally,
small penetrating arteries may be subject to lipohyalinosis,
leading to their gradual occlusion and producing a lacunar
syndrome.
Embolic infarctions
Emboli may be either cardiogenic (Caplan et al. 1983),
arising from the heart, or ‘artery-to-artery’ wherein they
arise from a thrombus on an arterial wall and travel downstream
to eventually plug a smaller caliber artery. The most
common cause of cardiogenic embolic infarction is atrial
fibrillation, wherein thrombi form within either the left
atrium or atrial appendage. Emboli are also seen in the sick
sinus syndrome; however, here the increased risk is probably
due to the associated atrial fibrillation. Atrial myxomas,
although rare, are very prone to fragment and undergo
embolization. Valvular disease is also associated with
emboli. In the case of mitral stenosis, this increased
risk may be related simply to the commonly associated
atrial fibrillation; however, in both infective endocarditis
(Anderson et al. 2003) and Libman–Sacks endocarditis, actual
embolization from the affected valves does occur. Prosthetic
valves may be complicated by thrombus formation with
embolization, and this is much more likely with mechanical
than with bioprosthetic valves. Myocardial infarction is
associated with thrombus formation and embolization,
both acutely and in the chronic phase. Acutely, thrombi
may form on the damaged endocardium, and the period of
risk here extends up through the first month or so post
myocardial infarction. Chronically, thrombi may form in
cases characterized by ventricular aneurysm or large areas
of reduced cardiac contractility. Another cardiac condition
favoring thrombus formation is dilated cardiomyopathy.
In all the foregoing cardiac conditions, emboli arise from
the left side of the heart: there is another condition, known
as ‘paradoxical embolization’ wherein emboli travel first
through the right heart. In these cases, one most commonly