Second edition

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bleed, presenting with dementia, incontinence, and gait
disturbance.
Other complications include arrhythmias and hyponatremia.
The hyponatremia, in turn, may be secondary to
either the syndrome of inappropriate ADH secretion
(SIADH), or, more commonly, cerebral salt wasting (CSW)
(Rabinstein and Wijdicks 2003). Differentiating SIADH
from CSW is critical, as the treatments are radically different.
In SIADH there is an increased release of ADH, with
consequent increased renal reabsorption of water leading to
hyponatremia in the setting of volume expansion. By contrast,
in CSW a release of natriuertic factors leads to renal
sodium and fluid loss and a hyponatremia in a setting of
volume contraction. SIADH is treated by fluid restriction,
whereas CSW is treated by the administration of saline.
INTRAVENTRICULAR HEMORRHAGE
Intraventricular hemorrhage presents in a fashion similar
to subarachnoid hemorrhage. Chronic communicating
hydrocephalus is a common sequela.
CEREBRAL VENOUS THROMBOSIS
Thrombosis of one of the dural sinuses (most commonly
the superior sagittal or the transverse sinus) may or may
not be followed by cerebral infarction, depending both on
whether drainage of a cerebral vein is blocked by the
thrombus and on whether or not the vein in question lacks
the anastamotic connections that might ensure adequate
venous drainage. When these unfavorable conditions are
met, venous congestion of the subserved area occurs with
the gradual appearance of a hemorrhagic infarction and
the appearance, clinically (Bousser et al. 1985; Cantu and
Barregarrementeria 1993; Gosk-Bierska et al. 2006), of the
gradual onset of headache, focal deficits appropriate to the
infarcted area, and, in a significant minority, seizures.
Thrombosis of the vein of Galen, although uncommon,
may be given special consideration here, given its clinical
expression. In these cases, the thalami, which are drained
by the internal cerebral veins, may undergo hemorrhagic
infarction, and this may result in stupor or coma (van den
Bergh et al. 2005) or, in milder cases, a subacute onset of
dementia (Krolak-Salmon et al. 2006).
Thrombosis of the superior sagittal sinus, by causing an
elevation of intracranial pressure, may cause symptoms even
in the absence of venous infarction, and patients may present
with the gradual evolution of headache and delirium.
Thrombosis of the cavernous sinuses produces a distinctive
syndrome with proptosis secondary to impaired
venous drainage from the eye, and ophthalmoplegia, secondary
to compression of the third and fourth cranial
nerves found in the wall of the sinus itself.
The evolution of symptoms seen with venous infarction
is very gradual, spanning days or even weeks. This leisurely
onset reflects the gradual propagation of the clot and the
equally gradual failure of collateral drainage.
SEQUELAE OF STROKE
7.4 Stroke 281
The sequelae of stroke include dementia, depression, anxiety,
and other sequelae, such as emotional incontinence, the
catastrophic reaction, the frontal lobe syndrome, and,
much less commonly, mania or psychosis.
Dementia
With multiple ischemic infarctions or intracerebral hemorrhages,
patients may be left demented. This may occur
with either cortical or white matter infarcts, producing a
multi-infarct dementia (discussed further in Section 10.1),
or with lacunes, producing a lacunar dementia (discussed
in Section 10.2). Typically, in such cases, one finds a history
of repeated stroke; however, occasionally, a ‘strategically’
placed single infarction or hemorrhage may leave the
patient with a dementia, as for example with infarcts or
hemorrhages within either temporal lobe or a hemorrhage
or lacune in the thalamus.
Subarachnoid hemorrhage may also be followed by a
dementia, due either to chronic hydrocephalus or multiple
infarctions due to vasospasm. When infarction is at fault,
one may find either a relatively small number of large vessel
infarcts or a myriad of ‘microinfarcts’ occurring secondary
to spasm of small vessels. CT scanning, although
quite capable of demonstrating the large infarcts, will miss
the smaller ones, and hence MRI may be required.
Cerebral venous thrombosis, if accompanied by multiple
venous infarctions, may also leave patients demented;
in the absence of these, most patients, if they survive, do so
without cognitive sequelae.
Post-stroke depression
In the weeks or months following stroke, close to one-half
of all patients will develop a depression of variable severity.
The location of the infarct or hemorrhage plays a part here,
with lesions in the anterior portions of the frontal lobes
being more likely to cause depression. Of interest, in cases
where the depression appears relatively early on, within
the first week or two, left frontal lesions are more likely,
whereas in cases where the onset is delayed for months,
lesions are found with approximately equal frequency in
either the left or the right frontal area. Depression has also
been noted with lesions of the left basal ganglia.
In evaluating a patient for possible post-stroke depression,
toxic and metabolic factors must also be considered.
Medications (e.g., metoclopramide or nifedipine) may
cause depression, and fatigue and loss of appetite are very
common with infections and certain metabolic disorders,
including hyponatremia and uremia.
Treatment with either citalopram (Anderson et al.
1994) or nortriptyline (Lipsey et al. 1984; Robinson et al.
2000) is effective; fluoxetine was found effective in one
study (Wiart et al. 2000) but not in another (Robinson
et al. 2000)
Of interest, given the frequency with which post-stroke
depression occurs, efforts have been made to determine if