1)CONGENITAL:

• MUCOPOLYSACCHARIDOSIS:

Caused-by lysosomal-enzyme-deficiencies, resulting in impaired glycosaminoglycan(GAG)-metabolism and subsequent intracellular-GAG-accumulation^[16]. The mechanism underlying PVS-enlargement in MPS remains unclear but has been observed in types -I, II, IIIA, IIIB, IIIC, and VI^[17-19].

Neuropathology: Hallmark-feature of MPS is the enlargement of the PVS, filled with a network of fibrous-tissue interspersed with cells-containing abnormal storage-material due to BBB-disruption and microvascular-leakage leading to perivascular-edema. Proposed theories attribute PVS-dilation either to abnormal-CSF-resorption at arachnoid-villi due to leptomeningeal-GAG-deposits or to direct-GAG-storage around vessels^[20]. While degree of PVS-enlargement depends on age and disease-subtype, it is not linked to clinical-severity^[21].

Imaging(MRI): PVS-dilation, commonly-symmetric,involving-5-regions: Periventricular-and-subcortical-white-matter,thalami,basal-ganglia,corpus-callosum,brainstem. Enlarged PVS can be seen in even in the absence of ventriculomegaly, representing an early-harbinger of impaired-CSF-dynamics, with ventriculomegaly developing later in the disease. Therefore, identifying PVS-enlargement on MRI could serve as a highly-sensitive surrogate-marker of abnormal-CSF-circulation in MPS^[17]. Additional-imaging-findings: shallow-J-shaped-sella-turcica,hydrocephalus,enlargement-of-subarachnoid-spaces,abnormal-periventricular-white-matter-changes,cortical-atrophy,cord-signal-changes-in-severe-cases.

Fig 5: FIGURE 5: MUCOPOLYSACCHARIDOSIS: IMAGES A (Axial) , B (Axial) and C (Sagittal) T2 W MR images show hallmark-feature of MPS- enlargement of the PVS within bilateral basal ganglia, subcortical white matter and corpus callosum (blue arrows)

• NEUROMELANOSIS(NM):

Neuropathology: Embryologically, melanocyte-precursors derived from neural-crest-cells normally migrate to leptomeninges^[22]. However NM involves an excessive accumulation, leading to visible-macroscopic-pigmentation. These melanocytic-cells can proliferate, infiltrate PVS, and occasionally undergo malignant-transformation into melanoma^[23].

Imaging(MRI): Paramagnetic melanin produce characteristic T1-hyperintensities, involving cerebellum, anterior and mesial-temporal-lobes,thalami, pons,medulla, reflecting melanocyte-accumulation in PVS along with possible diffuse-leptomeningeal-disease^[24,25].

Fig 6: FIGURE 6: NEUROMELANOSIS--> HYPOMELANOSIS OF ITO: IMAGES A (Axial) , B (Axial), C (Axial) FLAIR W MR images show hyperintense areas (blue arrows) within bilateral white matter with hypointense cysts within representing dilated PVS(white arrows). IMAGE D (Axial) T1 MR images show hyperintense signal within bilateral mesial temporal lobes representing accumulated melanin(orange arrows).

2)INFLAMMATORY-CONDITIONS:

• MULTIPLE-SCLEROSIS(MS):

Immune-mediated-condition leading to axonal-injury which starts with formation-of microglial-clusters within PVS--> proceed to myelin-loss, a process linked to plasma-fibrinogen-leakage, secondary to BBB-disruption^[26].

Neuropathology: Multifocal inflammatory-T-lymphocyte and macrophage-infiltration, oligodendrocyte and myelin-loss^[27-30].

Imaging(MRI): FLAIR hyperintense Demyelinating-plaques in perivenular-PVS-distribution, with size varying based on disease-stage; show contrast-enhancement during active-inflammation. Early-disease may show a "dot-dash"pattern of small FLAIR hyperintensities along lateral-ventricular-roof^[31]. With disease-progression, plaques extend further along medullary-perivenular-PVS, forming characteristic "Dawson fingers"^[31].The central-vein-sign(CVS) can help differentiate MS from other inflammatory-conditions^[32-33]. Additionally, MS patients tend to have higher burden of enlarged-PVS, significance of which remains uncertain.

Fig 7: FIGURE 7: MULTIPLE SCLEROSIS: IMAGES A (Axial FLAIR) and B (Sagittal FLAIR) MRI shows periventricular MS plaques secondary to perivenous inflammation along the axis of medullary veins (BLUE arrows) and resultant characteristic "Dawson's Fingers" sign (green arrows). IMAGE C- Axial SWI shows hypointense lines positioned centrally within the lesion, running entirely through the course of the lesions representing the "Central vein sign" (orange arrows). Image D- Schematic representation of “central vein sign” (purple arrows).

Fig 8: FIGURE 8: TUMEFACTIVE DEMYELINATION: IMAGES A (Axial FLAIR), B, C, D (CET1WI) MRI show non-enhancing tumefactive periventricular MS plaques secondary to perivenous inflammation along the axis of medullary veins (orange arrows). IMAGE B,C,D-Non enhancing hypointense linear foci noted running across centrally within the lesions, representing the inflamed and engorged medullary veins (blue arrows).

• NEUROSARCOIDOSIS:

Characterized by inflammation and formation of non-necrotizing-granulomas, affecting leptomeninges, +/- parenchymal-lesions and cranial-nerve-involvement^[34].

Neuropathology: Parenchymal-lesions reveal perivascular-lymphocytic-infiltrates, suggesting role of PVS in disease-spread^[35-37].

Imaging(MRI): Leptomeningeal-thickening and enhancement-->common, particularly in basal-cisterns^[38]. Parenchymal-lesions show infiltrative-perivascular-pattern, frequently near leptomeningeal-involvement, indicating that disease-dissemination may begin in leptomeninges^[36,39]. Deep-medullary-veins are enlarged on SWI in patients with PVS-enhancement and hydrocephalus^[40]. Vessel-wall-imaging(VWI)studies have revealed involvement of perforator-vessels and deep-medullary-veins, with biopsies from these patients frequently showing perivascular-granulomas^[37].

Fig 9: FIGURE 9: NEUROSARCOIDOSIS: IMAGE A- Axial SWI and IMAGE B- T1 contrast-enhanced images show asymmetrical tortuous medullary veins (green arrows) in the right frontal white matter region. A focus of intraparenchymal haemorrhage is seen in the left parietal region (yellow arrow).

• CHRONIC-LYMPHOCYTIC-INFLAMMATION-WITH-PONTINE-PERIVASCULAR-ENHANCEMENT-RESPONSIVE-TO-STEROIDS(CLIPPERS) and SUPRATENTORIAL-LYMPHOCYTIC-INFLAMMATION-WITH-PONTINE-PERIVASCULAR-ENHANCEMENT-RESPONSIVE-TO-STEROIDS(SLIPPERS):

Encephalomyelitis predominantly affecting brainstem,cerebellum,spinal-cord in CLIPPERS, and conversely basal-ganglia and cerebral-hemispheres in SLIPPERS.

Neuropathology: Perivascular-infiltration by CD3+T-cells. 

Imaging(MRI): Enhancing small, punctate, and curvilinear perivascular-lesions--> midbrain, medulla, subcortical-white-matter,cerebral-hemispheres with corresponding same-size on T2WI; however some lesions may not be visible on T2 or FLAIR-sequences^[41,42]. While other conditions, such as MS, can present with similar neuroimaging-features, CLIPPERS/SLIPPERS lesions are usually <3 mm, with no ring-enhancement or mass-effect, distinguishing them from larger, tumefactive MS plaques^[41]. If the T2-abnormality is significantly larger than the enhancing-component, other differential-diagnoses should be considered.

Fig 10: FIGURE 10: SUPRATENTORIAL LYMPHOCYTIC INFLAMMATION WITH PARENCHYMAL PERIVASCULAR ENHANCEMENT RESPONSIVE TO STEROIDS (SLIPPERS): IMAGES A (Sagittal), B (Axial), C (Coronal) Contrast enhanced T1 MR imaging show curvilinear foci of enhancement in bilateral cerebral white matter regions (blue arrows).

Fig 11: FIGURE 11: CHRONIC LYMPHOCYTIC INFLAMMATION WITH PARENCHYMAL PERIVASCULAR ENHANCEMENT RESPONSIVE TO STEROIDS (CLIPPERS): IMAGES A (Axial) - FLAIR and B (Axial) -Contrast enhanced T1 MR imaging show punctate and curvilinear enhancement (orange arrow) along patchy FLAIR hyperintensities (yellow arrow) involving pons, bilateral middle cerebellar peduncles and adjoining cerebellum.

• AUTOIMMUNE-GLIAL-FIBRILLARY-ACIDIC-PROTEIN-ASTROCYTOPATHY(AUTOIMMUNE-GFAP-ASTROCYTOPATHY):

Neuropathology: Centrum-semiovale, basal-ganglia, thalamus(GFAP rich areas)-->non-neoplastic mononuclear perivascular-infiltrates with frequent eosinophils, CD3-positive-T-lymphocytes, CD138-positive-plasma-cells, however without demyelination or vasculitic changes; with surrounding white-matter-gliosis and nonmonoclonal-plasma-cells^[43].

Imaging(MRI): MC->punctate or linear-enhancement within both basal-ganglia and thalamus. Other enhancement-patterns observed--> periventricular-radial-linear-enhancement and leptomeningeal-enhancement in brain&spinal-cord explained by gadolinium-leakage from damaged BBB^[43].

Fig 12: FIGURE 12: AUTOIMMUNE GLIAL FIBRILLARY ACIDIC PROTEIN (GFAP) ASTROCYTOPATHY: IMAGES A (FLAIR-Axial) and B (Coronal) and C (Sagittal) Contrast enhanced T1 MR images. Image A shows hyperintensities within periventricular, subcortical white matter and centrum semiovale (blue arrows). Image B and C show linear, perivascular pattern of contrast-enhancement (ornage arrows) extending radially from the periventricular surface and through the cerebral white matter consistent with Autoimmune GFAP astrocytopathy.

3)VASCULITIDES:

• PRIMARY-ANGIITIS-OF-CENTRAL-NERVOUS-SYSTEM(PACNS):

Neuropathology: Perivascular-lymphocytic-infiltration alongside vessel-wall-inflammation.

Imaging(MRI): MC abnormalities include T2/FLAIR hyperintensities or infarcts involving multiple-vascular-territories. Highly-variable-enhancement-patterns, including linear/perivascular, nodular, subependymal, or tumefactive-lesions that may mimic neoplasms^[44]. 

Fig 13: FIGURE 13: PRIMARY ANGIITIS OF CENTRAL NERVOUS SYSTEM (PACNS): IMAGE A -Axial DWI imaging and IMAGE B - Axial FLAIR imaging show multiple linear periventricular hyperintense foci (red arrows) demonstrating restricted diffusion (ADC not shown)- phenotype representing vasculitic infarcts. IMAGE C (Axial), D (Sagittal), E (Coronal) Contrast enhanced T1 MR imaging shows multiple linear foci of enhancement (yellow arrows) along PVS involving bilateral basal ganglia and cerebral white matter.

• MOYA-MOYA DISEASE:

Rare, chronic-vascular-disorder-of-unknown-cause, characterized-by-progressive bilateral-narrowing of the supraclinoid internal-carotid-arteries(ICAs) and proximal parts of middle and anterior-cerebral-arteries. 

"Moyamoya,"-means-puff-of-smoke,-describing-the-characteristic-appearance-of-abnormal-diffuse-proliferative-collateral-circulation-in-in-the-lenticulostriate-and-thalamocortical-perforating-arteries,-that-develop-secondary-to-ICA-obstruction,mimicking-enhancement-of-PVS-in-thalamus-and-striatocapsular-regions^[45,46]. Interestingly,large-vessel-occlusion-reduces-arterial-pulsations-->hindering-interstitial-bulk-flow,leads-to-PVS-enlargement-in-Moya-moya^[47].

Fig 14: FIGURE 14: MOYA-MOYA DISEASE: IMAGE A: Axial Contrast enhanced T1 MR imaging demonstrates that bilateral supraclinoid Internal Cerebral Arteries (blue arrows) are not visualized and replaced by numerous collaterals in basal cisterns. IMAGES B (Axial), C (Coronal), D (Sagittal) Contrast enhanced T1 MR imaging shows multiple abnormal proliferative lenticulostriate and thalamocortical collaterals (red arrows) and pial collaterals (yellow arrows). IMAGES E (Axial) and F (Sagittal) Time of Flight MR Angiography imaging shows replacement of bilateral distal supraclinoid ICA arteries by multiple abnormal perforator collaterals (blue arrows).

4)NEOPLASMS:

• PRIMARY-CNS-LYMPHOMA(PCNSL):

Typically intra-axial with an angiocentric-growth-pattern. 

Neuropathology: Large clusters of malignant-B-cells are seen around blood-vessels, and presence of these aggregates is linked to poorer-survival-rates.

Imaging: Hyperdense on CT owing to their dense-cellularity and generally show low-signal on T2WI and restricted-diffusion on MRI. In immunocompetent-patients, PCNSL-lesions-->intense, homogeneous and uniform contrast-enhancement. Conversely, necrotic-lesions are more common in immunocompromised-individuals. The angiocentric-growth-pattern may occasionally manifest on MRI as enhancing-lesions along PVS. A rare-subtype of PCNSL can present with intravascular-involvement, called as Angiocentric/Intravascular-lymphoma, which is associated with a more aggressive-course.

Fig 15: FIGURE 15: PRIMARY CNS LYMPHOMA - IMAGES A (Sagittal) and B (Coronal) Contrast enhanced T1 MR images show multiple solid homogeneously enhancing lesions oriented radially along the perivascular spaces (orange arrows)

Fig 16: FIGURE 16: ANGIOCENTRIC/ INTRAVASCULAR LYMPHOMA - Infarct like lesions and periventricular non specific white matter lesions - representing spread along perivascular spaces

• GLIOBLASTOMA:

Although,precise-mechanisms governing the proliferation of glioblastomas remain-unclear, recent-research indicates-that->glioblastomas may develop from perivascular-neural-crest-cells or lineages of radial-glia and their interactions with perivascular-cells and infiltration-through-these-pathways are thought to be critical in their development. Infiltration along perivascular-spaces may sometimes be noted extending from the main lesion on CET1WI^[48-50]. 

Glioma-progression disrupts->CSF-ISF exchange via reduced-astrocytic-AQP4-expression, leading to->inflammatory-cell-accumulation and impaired anti-tumor-immunity. PVS can serve as specialized-microenvironments where cancer stem-cells interact with growth-promoting-endothelial-cells contributing to tumor-progression;this interaction has been implicated in resistance to chemotherapy and radiation-therapy consequently forming basis for several-therapeutic-strategy-research-proposals to target these vascular-niches in treating->Glioblastomas^[48-50].

Fig 17: FIGURE 17: GLIOBLASTOMA MULTIFORME: IMAGES A (Sagittal) and B (Coronal)-Contrast enhanced T1 MR imaging show multiple punctate and linear foci of enhancement extending along the perivascular spaces from the main lesion (yellow arrows).

• CNS-METASTASES:

Metastatic-spread through PVS can occur either-by direct-seeding of metastases or through expansion from leptomeningeal-metastases. Perivascular-cells exhibit significant-plasticity and can undergo phenotypic-alteration -->crucial in establishing premetastatic-niches by formation of new-blood-vessels and stem-cell-proliferation that facilitate seeding and progression of metastatic-disease^[51].

Recent-research highlighted PVS-metastatic spread is associated with improved-survival-outcomes compared to traditional leptomeningeal-spread, hypothesized-to-have-been-linked-to antiangiogenic-therapies, suggesting a potential-escape-mechanism for tumor-cells as they-invade-along-PVS^[52-56].

Sometimes, focal-leptomeningeal-metastases arise from parenchymal-lesions via PVS-spread rather than through CSF-seeding,however this-necessitates-further-validation. Instances of perivascular-seeding and spread from CNS-metastases have-been-documented in lung-adenocarcinoma and breast-cancer; manifesting as linear, nodular, or miliary-enhancing-patterns on CET1WI, often localizing in subcortical&periventricular-white-matter, mimicking->vasculitis^[53-57].

Fig 18: FIGURE 18: CNS METASTASES - IMAGES A and B Contrast enhanced T1 -Axial MR images show multiple ring enhancing lesions along the perivascular distribution within bilateral basal ganglia (orange arrows) along with foci of leptomeningeal enhancement (blue arrows)

• DIFFUSE-LEPTOMENINGEAL-GLIONEURONAL-TUMOR(DLGNT):

Extensive-involvement-of-leptomeninges,-often-occurring-without-a-prominent-parenchymal-mass.

Imaging(MRI): Hallmark presence of numerous-small-subpial-cysts,thought-to-represent-enlarged-PVS: high-T2,low-T1-signal-and-FLAIR-signal-suppression; commonly found along temporal-and-inferior-frontal-lobes, less-commonly cerebellum,brainstem,spinal-cord;enabling distinction of DLGNT from other infectious/inflammatory-conditions with leptomeningeal-enhancement.

[fig]19[/fig]

• MULTINODULAR-VACUOLATING-GLIONEURONAL-TUMOR(MVNT):

Neuropathology:Grade-1-glioneuronal-tumors with large-gangliocytic-cell-clusters-within-cortex-&-subcortical-white-matter,accompanied-by-marked-perivascular-infiltration.

Imaging(MRI): Non-enhancing-nodular,coalescent-T2-hyperintense-clusters-that-however-do-not-suppress-on-FLAIR-unlike-enlarged-PVS,displaying-perivascular-arrangement;frequently-observed-in-frontal/parietal-lobes.

• LYMPHOMATOID-GRANULOMATOSIS(LYG):

Rare-lymphoproliferative-disorder,often-linked-to-Epstein-Barr-virus-infection-typically-presenting-with-lung-involvement-while-affecting-CNS-occasionally.

Neuropathology: Angiocentric-lymphoreticular-and-granulomatous-lesions,-with-abnormal-B-cell proliferation,significant-T-cell-infiltration-in-intravascular-and-perivascular-spaces,further-infiltrating-meninges,blood-vessels,brain-parenchyma^[58,59].

Imaging(MRI): Multiple-enhancing-T2/FLAIR-hyperintense-lesions-along-periventricular/subcortical-white-matter,with-restricted-diffusion,usually-distributed-along-medullary-vasculature;can-also-involve-brainstem,cerebellum,basal-ganglia,mimicking-other-conditions i.e.,CLIPPERS^[58-60].

Fig 20: FIGURE 20: LYMPHOMATOID GRANULOMATOSIS: IMAGE A (Coronal) and IMAGE B (Sagittal) Contrast enhanced T1 MR imaging shows linear enhancement along the intramedullary vessels involving bilateral cerebral white matter (yellow arrows). This patient did not show any evidence of nodular enhancing foci, mass forming lesions, or brainstem involvement.

• MENINGIOMA:

PVS Dysfunction-linked to peritumoral-edema in meningiomas, demonstrated by DTI-ALPS-studies^[61].

5)INFECTIONS:

• CRYPTOCOCCOSIS:

Neuropathology: Cryptococcus,having-strong-affinity-for-the-meninges, can-be-seen-within-macrophages-and-monocytes-in-leptomeningeal-capillaries-and-endothelial-cells, where-it-disrupts-BBB and invades-CNS^[62-63].

Imaging(MRI): Meningoencephalitis, cerebral-edema, leptomeningeal-enhancement, varying depending on host's-immune-response^[64]. Dilated-PVS seen in basal-ganglia, periventricular&subcortical-white-matter, centrum-semiovale;associated-with poorer-outcomes and progression to cryptococcal-meningoencephalitis, characterized by formation of cryptococcomas. Dilated-PVS merge into gelatinous-pseudocysts forming cryptococcomas, containing large-number-of-organisms, exhibiting varying-T2-signal-intensities on-MRI depending on their protein-content, showing ring-shaped/intense-solid-contrast-enhancement^[65,66].

Fig 21: FIGURE 21: CRYPTOCOCCOSIS- In a 57 year old male with HIV since 12 years and sudden onset headache since 3 days , MR imaging of the brain shows: IMAGE A : Axial FLAIR MR image shows patchy hyperintense areas (red arrows) involving bilateral basal ganglia region with perifocal edema. IMAGES B (Axial), C (Coronal), D (Sagittal): Contrast enhanced T1 MR images show nodular foci of enhancement (yellow arrows) corresponding to cryptococcomas , radially oriented along the PVS. IMAGE E (Axial) shows ependymal enhancement along the 4th ventricle (blue arrows).

• NEUROSYPHILIS:

Neuropathology: Inflammatory-infiltrates-with-lymphocytes-and-plasma-cells-along-PVS, small-vessel-proliferation-with-obliterative-endarteritis-around-regions-of-necrosis.

Imaging(MRI): Leptomeningeal-enhancement-with-enhancing-gummas-arising-adjacent-to-meninges; meningoencephalitis-and-cerebral-edema. 

Fig 22: FIGURE 22: NEUROSYPHILIS- IMAGE A (Axial), B (Coronal), C(Sagittal), D(Coronal) Contrast enhanced T1 MR imaging shows multiple nodular and linear foci of enhancement along PVS involving bilateral basal ganglia and cerebral white matter (yellow arrows). IMAGE E (Axial) Contrast enhanced T1 MR imaging shows multiple nodular foci of enhancement along the leptomeninges representing syphilitic gummas (red arrows).

• LYME DISEASE/NEUROBORRELIOSIS:

Neuropathology: Accumulation-of-spirochetes-within-vascular, perivascular, and extravascular-compartments-along-with-interstitial-and-perivascular-lymphocytic-infiltrates.

Imaging(MRI): Multifocal-subcortical&periventricular-white-matter-lesions,dilated-PVS,PVS-enhancement-with-distribution-pattern-resembling-CLIPPERS.

6)NEURODEGENERATIVE CONDITIONS:

• ALZHEIMER'S-DISEASE:

PVS-enlargement-in-centrum-semiovale-is-associated-with-elevated-AD-CSF-biomarkers-phospho-tau(p-t),total-tau(t-t)-and-neurogranin-in-patients-with-increased-CSF-amyloid-β-levels;AD-related-cognitive-decline and positive-results-on-fluorine-18[18F]-florbetaben-PET-imaging^[67,68]--> Extent-of-PVS-enlargement-in-centrum-semiovale-may-reflect-amyloid-β-burden hypotherized to occur because a fraction of amyloid-β peptides are cleared through interstitial-bulk-fluid-flow along PVS^[69,70].

Fig 23: FIGURE 23: ALZHEIMER'S DISEASE: Images A, B ( Axial sections of T2 MRI) shows multiple dilated PVS in bilateral subcortical white matter regions (blue arrows); Relative cortical atrophy of bilateral parietal regions (orange arrows); Multiple patchy T2 hyperintense areas in bilateral periventricular and deep white matter regions (green arrows).

• CEREBRAL-AMYLOID-ARTERIOPATHY(CAA):

Characterized-by-abnormal-deposition-of-amyloid-β-in-cortical&leptomeningeal-arteries-and-arteriolar-perivascular-spaces(PVS);linked-to-increased-risk-of-intracranial,predominantly-lobar-hemorrhages(cortical-subcortical-regions).Like-AD,CAA-is-associated-with-enlarged-PVS-in-centrum-semiovale. Although-higher-incidence-of-severe-PVS-enlargement-has-been-found-in-patients-with-CAA-related hemorrhages(44%)compared-to-those-with-hypertensive-hemorrhages(18%),enlarged-PVS-in-centrum-semiovale-is-quite-nonspecific-and-can-also-occur-with-aging^[71]. Conversely,enlarged-PVS-in-basal-ganglia-is-more-commonly-seen-in-hypertensive-arteriopathy^[71]. Severely-enlarged-PVS-in-centrum-semiovale-and-multifocal-white-matter-lesions-now-form-part-of-->"Boston-criteria-v2.0",as-additional-features-for-diagnosing-probable-or-possible-CAA,in-the-context-of-lobar-hemorrhages-and-absence-of-deep-hemorrhagic-lesions^[72]. Glymphatic -flow impairment leads to dilated-PVS in Ischemia/Stroke^[77].

Fig 24: FIGURE 24: INFLAMMATORY CEREBRAL AMYLOID ANGIOPATHY (CAA): Images A, B (Axial sections of FLAIR MRI) and Image D (Axial T2WI) show asymmetric white matter hyperintensities extending upto the subcortical white matter (orange arrows) with enlarged PVS within the involved regions (blue arrows). Image C ( Axial SWI) shows multiple lobar microhemorrhages ( purple arrows) in bilateral hemispheres.

Fig 25: FIGURE 25: HYPERTENSIVE MICROANGIOPATHY: Image A (Axial FLAIR MRI) shows bilateral periventricular white matter hyperintensities (green arrow) and Image B (Axial T2WI) shows enlarged PVS within the involved regions (blue arrows). Image C ( Axial SWI) shows multiple microhemorrhages in the deep grey matter (orange arrow)

Fig 26: FIGURE 26: STROKE: Images A, B and C ( Axial sections of FLAIR MRI) show gliosis and volume loss involving left frontoparietal lobes with dilated PVS ( blue arrows). Image D- TOF MRA shows absent flow related signals in left Internal carotid artery and Anterior cerebral artery(orange arrow).

• PARKINSON'S-DISEASE:

Linked-to-degeneration-of-dopaminergic-neurons-and-deposition-of-alpha-synuclein-in-perivascular-basement-membranes. DTI-ALPS-studies-have-shown-glymphatic-system-dysfunction,suggesting-that-PVS-burden-may-serve-as-a-potential-disease-biomarker^[73]. Enlarged-PVS-in-basal-ganglia-has-been-linked-to-worsening-motor-symptoms-in-PD,alongside-reduced-dopamine-transporter-function-seen-in-^[123I]ioflupane-scans^[74]. 7T-MRI-studies-have-found-greater-PVS-burden-in-PD-patients,correlating-with-freezing-gait-and-higher-levodopa-doses. Patients-with-tremor-dominant-PD-tend-to-have-lower-PVS-burden,and-are-less-responsive-to-dopaminergic-treatment^[75,76].