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Taste and Smell and the Basal Ganglia
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Taste and Smell and the Basal Ganglia

I have had two brain MRI's in the last five months, both done with gadolinium contrast.  The MRI's were performed by separate establishments and examined by different physicians trained to interpret MRI's.

In both cases, the physicians noted a "prominient perivascular space in the left inferior basal ganglia." The oval area on the MRI measured 8mm.  However, since such a "Virchow-Robin" space is considered benign, the two MRI's ultimately were classified as "normal."

Here's the problem:
I suddenly lost much of my sense of taste and smell during the acute onset of several symptoms that prompted these brain MRI's.  I understand that some portion of taste and smell interpretation is processed in the basal ganglia in addition to its primary function of handling motor functions. It is also a fact that people suffering from Parkinson's disease also note a decreased ability to taste/smell early in the disease's course.

Could this "perivascular space" actually be the root cause of my taste/smell dysfunction --perhaps disrupting dopamine production and therefore dampening the ability of my brain to interpret taste and smell? My main concern is that this perivascular space is actually something not nearly as benign as the doctors are being led to believe. While I understand these spaces are pretty common in older adults, wouldn't it seem unusual for an 8mm space to show up in a 35-year-old?
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Virchow Robin spaces are just as common in younger people, there is no age related difference. It is not a space where brain tissue previously was either, so the surroundig strucute of the brain is normal.

Primary taste and smell senses should not be affected with just a lesion of the basal ganglia, other regions would need to be affected - such as the oflactory plate at the middle front of the skull for smell or the brainstem. The most common causes of loss of taste and smell are peripheral (that is, outside the central nervous system). For instance an infection or viral infection can damage the receptors and their nerve endings for taste and smell. Unless you have a primary neurotransmitter problem this would not be a functional cause of the symptoms either (for instance dopaminergic activity in PArkinsons
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