Intracranial vasculopathies caused by virus and bacterial infection

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Varicella zoster virus vasculopathy

Varicella zoster virus (VZV) vasculopathy may often be clinically silent but may present with stroke and can be diagnosed because of the following symptoms, signs and findings (for review: Nagel et al. [28]).

(1) About two-thirds of patients have a history of zoster rash, particularly ophthalmic-distribution zoster or a history of chicken pox. There is a delay between the onset of zoster/chicken pox and the onset of stroke averaging 4.1 months (range between same day and 2.5 years). But about one-third of patients with a pathologically and virologically verified disease have no history of zoster rash or chicken pox.

(2) Angiographic evidence of narrowing in cerebral arteries may be found in MR angiography. In vascular studies 70% had vasculopathies. Different patterns of vascular lesions have been found. There was pure large artery disease in 13%, pure small artery disease in 37% and a mixed vascular pathology in most patients (50%). (3) Varicella zoster virus as the cause of stroke can be proven by examinations of the cerebrospinal fluid: 67% of patients have a pleocytosis (>5 white blood cells/mm3). Thus, some patients may even have no pleocytosis. Specific antibodies (anti-VZV-IgG) with proven intrathecal synthesis were found in 93% of patients, and VZV-DNA in 30%.

A negative result for both VZV DNA and anti-VZV-IgG antibody in CSF can reliably exclude the diagnosis of VZV vasculopathy.

Chronic bacterial, meningeal infections

Ischemic stroke complicates chronic meningeal infections which cause inflammation and thrombosis of arteries and veins on the surface of the brain. With tuberculous meningitis, infection is predominantly located at the base of the brain and vasculitis causes thrombosis in the large intracranial arteries and territorial infarction. Different vascular territories may be involved depending on the spatial extent of the men-ingeal infection. Tuberculous meningitis has to be considered as a clinical syndrome when one of the following criteria accompanies ischemic stroke [29]:

• medical history with manifestation of tuberculosis in the lungs or in a different organ (this manifestation may have been many decades ago)

• one or more symptoms indicating chronic meningeal infection such as headache or subfebrile temperature preceding stroke

• other signs indicating a process in the basal meninges such as lesion of cranial nerves or development of hydrocephalus as a consequence of an obstruction of the basal cisterns.

In addition there may be more unspecific signs as well, such as loss of appetite, drowsiness or myalgia. Contrast-enhanced magnetic resonance imaging may show up the basal meningitis. The cerebrospinal fluid shows mild to moderate pleocytosis with white blood cells up to 300/mm3, the glucose is reduced with subacute infections and protein is elevated as a sign of the disturbed circulation of the cerebrospinal fluid. Infection with tuberculosis can be proven by cytology (Ziehl-Neelsen), culture, detection of DNA (PCR) or antigen.

Syphilitic meningovasculitis

Syphilitic meningovasculitis may be the first clinical presentation of an infection with Treponema pallidum. The primary infection with a syphilitic lesion in the mucosa may have been months to years ago. Syphilitic meningovasculitis presents with an obliteration of small or middle-large vessels; rarely are large arteries involved. The territory of the middle cerebral artery is mainly involved. Infected vessels and their vasa vasorum together with lymphocytic infiltration cause a slow progression of stenosis leading to occlusion.

Intracranial Infection

Figure 9.7. Meningovascular syphilis. The patient presented with the following signs: awake but apathic, decreased episodic memory, complete upgaze palsy, incomplete downgaze palsy, disturbed converge of eyes, contraversive ocular tilt reaction (tendency to fall to the right side and skew deviation). Pupils were reactive to light. There was a minimalhemiparesis shown up by a tendency to pronate with the right arm. MR shows a vascular lesion in the territory of the left thalamic-subthalamic artery. This lesion was caused by meningovascular syphilis proved by intrathecal production of specific antibodies (FTA-Abs) and mild pleocytosis.

Figure 9.7. Meningovascular syphilis. The patient presented with the following signs: awake but apathic, decreased episodic memory, complete upgaze palsy, incomplete downgaze palsy, disturbed converge of eyes, contraversive ocular tilt reaction (tendency to fall to the right side and skew deviation). Pupils were reactive to light. There was a minimalhemiparesis shown up by a tendency to pronate with the right arm. MR shows a vascular lesion in the territory of the left thalamic-subthalamic artery. This lesion was caused by meningovascular syphilis proved by intrathecal production of specific antibodies (FTA-Abs) and mild pleocytosis.

Patients may present with signs of meningeal (meningo-encephalitic) inflammation such as headache, dizziness, feeling sick, sleep disorder, change of personality, apathy and deficits of episodic memory. Ischemic stroke can be preceded by TIA. Usually, the size of ischemic infarcts is small. There may be lesions of the cranial nerves because of the associated meningitis (Figure 9.7). Documentation of the intrathecal production of specific antibodies is required for a definite diagnosis of syphilitic meningovasculitis. Pleocytosis in the CSF together with specific antibodies in the serum can be taken as evidence of a likely syphilitic meningovasculitis. Other mechanisms of stroke associated with syphilis are mesaaortitis luetica with aortic dissection and endocarditis.

Viral and bacterial infections can cause specific vasculopathies.

Intracranial Infection

Figure 9.8. CADASIL. Extensive morphological abnormalities are found in CADASIL despite the absence of vascular risk factors, particularly in younger patients. White matter hyperintensities (WMHs) are characteristically located in the white matter of the anterior temporal lobe and the externalcapsule, which is unusualfor other small-vesseldiseases. (Courtesy of Professor Franz Fazekas, University of Graz.)

Figure 9.8. CADASIL. Extensive morphological abnormalities are found in CADASIL despite the absence of vascular risk factors, particularly in younger patients. White matter hyperintensities (WMHs) are characteristically located in the white matter of the anterior temporal lobe and the externalcapsule, which is unusualfor other small-vesseldiseases. (Courtesy of Professor Franz Fazekas, University of Graz.)

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