CSVT can also be caused by infections or dehydration. Hemorrhagic strokes (HS) may be intraparenchymal (primary, or secondary bleeding after AIS) or associated with intra-ventricular, subarachnoid, subdural, or epidural bleeds. The most common causes of HS are vascular malformations, head trauma, and vasculitis.
The acute onset of focal neurologic deficits in a child is strokeuntil proven otherwise. Symptoms may be subtle and nonspecific, which can lead to a delay in diagnosis. AIS typicallypresents with acute, focal neurologic deficits. Hemiparesis ismost common, but visual, speech, sensory, or balance deficits may be present. Unlike AIS in adults, focal seizures arequite common in childhood presentation of AIS. Similarly,neonatal AIS most often presents with acute symptomatic focal seizures (typically in the first day of life) or withencephalopathy.
Symptoms of CSVT may progress more gradually and be more variable and nonspecific than AIS. In CSVT, acute focal deficits may be present, or the child may have progressive signs of elevated intracranial pressure, including headache, papilledema, diplopia (most often from cranial nerve VI palsy), seizures, lethargy, or confusion.
HS tends to present acutely, with a sudden “thunderclap” headache. HS may also present with loss of consciousness, nuchal rigidity, focal deficits, or seizures and can be rapidly fatal.
Congenital hemiplegia becomes apparent as infants develop, with decreased use of one side of the body, early handedness, or ignoring one side. Neuroimaging reveals an area of encephalomalacia in the contralateral cerebral hemisphere. The details of the child’s intrauterine, labor, delivery, and postnatal history often are unremarkable. The area of encephalomalacia may predispose the child to epilepsy.
There are many conditions that mimic pediatric stroke, most of which are more common than AIS, HS, or CSVT. Some of these mimics are benign (migraine, psychogenic weakness, musculoskeletal abnormalities), but others require specific, prompt diagnosis and/or treatment (e.g., transient postictal weakness, intracranial infection, inflammatory disease of the central nervous system, tumor, or posterior reversible leukoencephalopathy syndrome).
On initial presentation, acute neuroimaging is necessary. A noncontrast head computed tomography (CT) scan is highly sensitive to acute HS and can reveal larger, mature AIS; acute, nonhemorrhagic stroke may not be seen on routine CT. Therefore, MRI with diffusion-weighted imaging is required for most presentations. Angiography by magnetic resonance angiography (MRA) or CT angiography is used to confirm arterial occlusion in AIS and can identify underlying arteriopathy, vascular malformations, and aneurysms. Diagnosis of CSVT requires a high clinical suspicion and purposeful imaging of the cerebral venous system with venography by MRI or CT. If clinical assessment does not reveal the cause of the stroke, a complete laboratory investigation should be undertaken promptly based on suspected etiologies (see Table 182-5). Many children with AIS have more than one predisposing factor, so identifying one risk factor does not obviate the need for a complete evaluation.