Morphology and pathogenesis
Pathological changes in the cerebral microvasculature develop along two main pathways, depending on the caliber of the involved arteries. Occlusion of relatively large penetrating vessels leads to the formation of localized areas of necrosis — lacunar infarcts (lacunar infarcts). If smaller terminal arterioles are blocked, diffuse chronic ischemia develops. Morphologically, this manifests as ischemic demyelination and proliferation of supportive tissue — gliosis.
The distribution of lesions is variable, but changes are most frequently localized in deep brain structures. The thalamus, basal ganglia, ventral pons, as well as the periventricular and deep white matter, are primarily affected.
Imaging findings: CT vs MRI
Computed tomography has low sensitivity in the early stages of the disease. A classic, albeit non-specific, CT sign of the chronic process is leukoaraiosis (leukoaraiosis) — diffuse hypodensity (decreased X-ray attenuation) of the white matter. Differentiating a fresh acute infarct from an old scar on CT is extremely difficult.
Magnetic resonance imaging is the undisputed method of choice. The DWI (diffusion-weighted imaging) sequence allows for the precise localization of acute infarcts, which are frequently clinically "silent" and detected incidentally. The FLAIR sequence clearly visualizes the evolution of lesions:
- Acute stage: rounded zones with indistinct borders.
- Subacute stage: lesion size is unstable, frequently increasing in volume.
- Mature lacuna: appears as a well-defined cavity less than 1.5 cm in diameter. On FLAIR, a hyperintense glial rim is clearly visible around it, allowing reliable differentiation of the lacuna from a physiologically enlarged perivascular space.
Microbleeds and their patterns
Microhaemorrhages (microhaemorrhages) are a critical marker of capillary fragility. Epidemiologically, they occur in approximately 6% of elderly individuals without neurological symptoms. They are completely invisible on unenhanced CT. To detect them, MRI sequences sensitive to magnetic susceptibility and hemosiderin deposits are used.
The sensitivity of the sequences increases in the following order: baseline T2 spin-echo -> DWI -> gradient echo T2* GRE -> SWI (susceptibility-weighted imaging). On SWI, microbleeds appear as multiple pronounced hypointense (black) dots.
The topography of the lesions directly points to the probable etiology:
- Hypertensive microangiopathy: hemorrhages are predominantly localized in the deep grey matter nuclei.
- Amyloid angiopathy (amyloid angiopathy): the lesion pattern shifts to the periphery, with a typical lobar distribution.
Causes of microangiopathies
Diseases affecting small vessels are divided into groups by frequency of occurrence:
- Frequent: ischemic microangiopathy and vasospasm secondary to subarachnoid hemorrhage (SAH).
- Infrequent: intracranial atheromatosis, various vasculitides, amyloid angiopathy, radiation vasculopathy, sickle cell anemia, and consequences of drug-induced hypertension.
- Rare: syndromes with a specific MRI presentation. For example, autosomal dominant arteriopathy CADASIL (affecting the anterior temporal lobes), Susac syndrome (rounded lesions in the corpus callosum), intravascular lymphoma, Fabry disease, and Moyamoya occlusive vasculopathy (Moyamoya, characterized by a pathological collateral network resembling a "puff of smoke" on angiography).
Briefly: answers to topical questions
What are the characteristic MRI features and lesion localization in CADASIL syndrome and Susac syndrome?
The characteristic MRI features and lesion localization in these syndromes include specific changes in the white matter and corpus callosum.
- CADASIL — extensive confluent white matter signal abnormality zones. Typical localization involves the anterior temporal lobes and subinsular regions, frequently with basal ganglia involvement and the presence of microhaemorrhages.
- Susac syndrome (retinocochleocerebral autoimmune vasculopathy) — small multifocal, often round lesions in the corpus callosum.
What are the angiographic and pathogenetic features of occlusive moyamoya vasculopathy?
Moyamoya occlusive vasculopathy is an idiopathic arteriopathy characterized by the development of collaterals against the background of progressive vascular occlusion.
- Pathogenesis — terminal occlusive vasculopathy in which collaterals develop secondarily due to progressive occlusion of the supraclinoid internal carotid arteries (ICAs). The process often extends to the proximal segments of the anterior and middle cerebral arteries.
- Angiographic presentation — visualization of abnormal, dilated, and irregular collateral vessels resembling a «puff of smoke» (puff of smoke). On MR angiography (TOF MRA), there is a signal void from blood flow in the terminal segments of the internal carotid and middle cerebral arteries, while multiple small abnormal collaterals are revealed in the anterior perforated substance and the left choroidal fissure.
To remember microhemorrhage patterns, use the rule: «Hypertension hits Deep (basal ganglia), while Amyloid hits High and at the edges (lobar cortical distribution)».
Class and exam questions
Can microhemorrhages in small vessel disease be seen on CT?
No, microhemorrhages are not visualized on native CT. Their detection requires MRI sequences sensitive to magnetic susceptibility artifacts (SWI or T2*).
How to differentiate an old lacune from an enlarged perivascular space on MRI?
On FLAIR MRI, a mature established lacune is always surrounded by a characteristic hyperintense glial rim. An enlarged perivascular space lacks such a rim.
What is the clinical danger of multiple microhemorrhages?
They serve as a marker of pronounced vascular wall fragility. Their presence significantly increases the risk of massive parenchymal brain hemorrhage, especially if the patient is prescribed aggressive antiplatelet therapy.
What else to study on this topic
- MRI patterns of rare genetic vasculopathies (CADASIL, Fabry disease)
- Susac syndrome: clinical triad and specific corpus callosum lesions
- Moyamoya disease: pathogenesis, collateral circulation, and secondary patterns
- Vessel Wall Imaging technique in vasculitis
- Radiodiagnosis of cerebral venous and sinus thrombosis («empty delta sign» on CT)
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