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|LETTER TO EDITOR
|Year : 2014 | Volume
| Issue : 3 | Page : 334-335
Giant dilations of perivascular spaces in deep brain locations: A cause for Parkinsonism?
Baran Yilmaz1, Zafer Orkun Toktas1, Murat Sakir Eksi2, Hayal Ergin Toktas3, Fusun Mayda Domac3, Turker Kilic1
1 Department of Neurosurgery, Bahcesehir University Medical School, Istanbul, Turkey
2 Department of Orthopedics Spine Center, University of California, San Francisco, California, USA
3 Department of Neurology, Erenkoy Mental Research and Training Hospital, Istanbul, Turkey
|Date of Submission||03-Jun-2014|
|Date of Decision||10-Jun-2014|
|Date of Acceptance||10-Jun-2014|
|Date of Web Publication||18-Jul-2014|
Murat Sakir Eksi
Department of Orthopedics Spine Center, University of California, San Francisco, California
Source of Support: None, Conflict of Interest: None
|How to cite this article:|
Yilmaz B, Toktas ZO, Eksi MS, Toktas HE, Domac FM, Kilic T. Giant dilations of perivascular spaces in deep brain locations: A cause for Parkinsonism?. Neurol India 2014;62:334-5
|How to cite this URL:|
Yilmaz B, Toktas ZO, Eksi MS, Toktas HE, Domac FM, Kilic T. Giant dilations of perivascular spaces in deep brain locations: A cause for Parkinsonism?. Neurol India [serial online] 2014 [cited 2020 Jan 29];62:334-5. Available from: http://www.neurologyindia.com/text.asp?2014/62/3/334/137022
Virchow-Robin or perivascular spaces (PVSs) are pia-mater lined zones that surround vessels penetrating in and out of brain parenchyma. Virchow-Robin spaces with diameter of >1.5 cm 3 are termed as giant variants.  Giant PVS can be misdiagnosed as cystic lacunar infarcts, cystic tumors, and cystic infections especially when there are associated neurologic symptoms. We presented a patient with bilateral basal ganglia giant PVS and Parkinsonism.
A 54-year-old right-handed woman presented with asymmetric tremor, markedly in the right hand and difficulty to walk for 1 year duration. Neurological examination revealed mild facial masking, decreased blink rate, hypophonia, decreased arm swing on the right, 4-6 Hz bilateral resting tremor and cogwheel rigidity distinct on the right side, bradykinesia, and difficulty in walking. Handwriting was small and became smaller as she continued to write. Pull test was positive without recovery. Total Unified Parkinson's Disease Rating Scale (UPDRS) score was 36. There were no other risk factors or features for seconday Porkinsonism. Computed tomography (CT) revealed multilobular cysts without calcification in bilateral basal ganglia, [Figure 1]a. Magnetic resonance imaging (MRI) demonstrated multilobular cysts in the basal ganglia, periventricular white matter, and centrum semiovale bilaterally. The cysts were isointense to cerebrospinal fluid (CSF) on all MRI sequences [Figure 1]b-f with no contrast enhancement [Figure 1]c. There was no hydrocephalus, but mass effect was evident in the tissues adjacent to the cysts [Figure 1]b, d-f. MR-angiography was negative for vascular malformations. Comprehensive work-up for any central nervous system infections was negative. Based on this data a final diagnosis of giant perivascular space was considered. She was put on dopamine agonist, pramipexol 3 × 0.125 mg initialy and was gradually titrated to 3 × 1 mg. At 10 months of follow-up, she had significant improvement in her symptoms and UPDRS score was 11.
|Figure 1: Computed tomography shows hypodense cystic areas in both basal ganglia. Neither cyst has calcifi cation (a). Fluid-attenuated inversion recovery (FLAIR) and T2-weighted magnetic resonance images reveal multilobular cysts that are isointense to cerebrospinal fl uid and located in the basal ganglia, periventricular white matter, and centrum semiovale. Note the pericystic edema on the FLAIR images (b,d-f). On T1-weighted scans, cysts do not enhance with intravenous gadolinium (c)|
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Perivascular spaces are fluid filled spaces around vascular structures. Rudolf Virchow (German pathologist) and Charles Philippe Robin (French anatomist) described PVS in the years 1851 and 1859, respectively.  Structure of PVS differs whether they accompany arterial or venous vessels and whether their location is superficial or deeper in the brain.  Perivascular spaces are too thin in diameter (only 1-2 mm), however they have more easily been detected after invention of high resolution T2-weighted MRI. Although there have been numerous arguments about nature of the fluid in PVS, today it has been accepted that these spaces function as drainage pathways for brain interstitial fluid and have some immune defense mechanisms by harboring microglia inside.  On MRI, PVS dilations are isointense to CSF in imaging sequences with no contrast enhancement. ,, They are well circumscribed and follow lenticulostriate arteries in anterior perforated substance, perforating arteries in the white matter and penetrating branches of collicular and accessory collicular arteries in midbrain. ,
Differential for PVS includes cystic lacunar infarctions, cystic tumors and cystic infections.  Cystic lacunar infarcts have similar image intensities like dilated PVS as they contain water. Cystic infarctions are more common in white matter, whereas dilated PVS present usually in basal ganglia. Cystic infarctions have slit-like or ovoid shape, dilated PVS are round or linear.  On CT image, dilated PVS do not have calcifications, whereas they may be a feature of parasitic infestations. As in our case, laboratory tests also help to differentiate dilated PVS from infections. As a confounding matter, hyperintensity observed around some dilated PVS, which makes us think tumor diagnosis, sometimes delays the diagnosis. However, these fields can be distinguished as gliotic regions with new MRI technologies (MR spectroscopy).
Presenting clinical features of giant PVS depend on the location of the PVS. Giant PVS present near CSF pathways like in mesencephalon and brain stem, may present with hydrocephalus.  Hydrocephalus develops insidiously and the clinical presentation may mimic normal-pressure-hydrocephalus. Management with CSF diversion surgeries (V-P shunt, cystoperitoneal shunt, ventriculocisternostomy) alleviates signs and symptoms even though cyst size generally does not change.  There has been case reports relating seizure disorder to PVS; however, the relationship is uncertain.  Bastos et al. described a 64-year-old man with PVS dilation in hypocampal region, who presented with temporal lobe seizure.  Patient with PVS and seizure disorder should be evaluated comprehensively before the causal relation between them is considered Multiple enlarged PVS in striatum, or état criblé, has been related with arteriosclerotic Parkinsonism.  However, the underlying mechanism has not been outlined, yet. An explanation in this patient can be the location of giant PVS in the basal ganglia. Bilateral compression of extrapyramidal pathways might have resulted in Parkinsonism signs and symptoms. After dopamine agonist therapy, clinical findings regressed gradually. In this patient, one cannot exclude the possiblity of occurrence of the two diseases in the same patient. However, clinical rarity of the condition prevents large-scale prospective studies to be conducted.
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