STRANGE MRI RESULTS!! All MP, please, your thoughts?

Discussion in 'Fibromyalgia Main Forum' started by karinaxx, Mar 13, 2007.

  1. karinaxx

    karinaxx New Member

    Hi to everyone,

    we made it to Switzerland (on the way, made a MRI in Bombay)
    It was a long and exhausting journey, both of us, my son and myself are in a bad flare and i am hardly able to walk more than 300m , than i have to rest, and usually coming home and colapse with pain and total exhaustion.
    But the good side, the cool clima feels good.

    Any way, i just got the MRI results and there is something strange going on and i have an appointment with a Neurologist in two days. Any thought on this?

    "A small incidental venous angioma is seen in the right retro-lentiform region extending medially upto the ventricular trigone"

    I checked it out and landed again in the area of Vascular Deseases. One of the test i wanted my doc to do, was the ANCA, (Wagners D.and other vascular d.s), so most probably i will get this done now.
    Any thoughts on Vascular D.?

    Strange thing is the most common reason for such deseases seems to be viruses; parvovirus keeps poping up!


    here some info i found :
    What is a venous angioma (Developmental Venous Anomaly, DVA)?
    How common are venous angiomas?
    Why do venous angiomas develop?
    What are the symptoms of venous angiomas?
    More about venous angioma hemorrhage.
    What are the complications of venous angiomas?
    How are venous angiomas detected?
    How are venous angiomas treated?


    1. What is a venous angioma (Developmental Venous Anomaly, DVA)?

    A venous angioma, also referred to as a "developmental venous anomaly" (DVA) or sometimes "venous malformation" is basically an extreme variation of veins draining normal brain tissue in that region. That is, a venous angioma (DVA) by itself is not necessarily "abnormal"; it's rather a variation of normal. However, having stated this, it should be noted that some studies have found that some veins (or all veins) that comprise a venous angioma have structural abnormalities compared with more normal veins. Regardless, most neurosurgeons regard venous angiomas by themselves as extreme variations of normal venous drainage.

    The veins that comprise a venous angioma usually form a little cluster ("star burst" or "caput Medusae" - looks like a "head of snakes"), and these veins generally drain into a larger "collector" vein. The collector vein is usually on the surface of the brain, but sometimes there may be deep drainage too. The pattern (arrangement) of these veins is frequently simple, but may at times be more complex looking. Between the veins that make us the venous angioma is normal brain tissue. Sometimes one or more of these veins can appear extra dilated and may be more thin walled than other veins in the brain. Venous angiomas tend to occur near the frontal horns of the ventricles (fluid filled spaces of the brain) and also in the cerebellum (small part of the brain at the lower back part of the head).

    Importantly, venous angiomas are frequently associated with cavernous malformations (cavernomas) and it is through this association that trouble potentially arises ( take me to the section on Cavernomas now). Venous angiomas on their own don't tend to cause any trouble and, with few (reported) exceptions, should generally be left alone (see Section 8., below).

    2. How common are venous angiomas?

    The true prevalence of venous angiomas is not known, but autopsy series indicate that they are much more common than cavernous hemangiomas, aneurysms and arteriovenous malformations. The prevalence of venous angiomas (i.e., their presence at any one time in the general population) is probably somewhere between 5-10%; it is higher in imaging series compared with autopsy series. Venous angiomas therefore represent the most common blood vessel (vascular) "anomaly" in the central nervous system.

    3. Why do venous angiomas develop?

    There are no well established risk factors for venous angioma formation. They are thought to be nonhereditary (i.e., not inherited from your parents). Venous angiomas are considered "congenital anomalies", i.e., persons are born with these lesions, they don't simply "develop" these in later life. Some venous angiomas may themselves undergo evolutionary changes over the years that they are observed (i.e., the lesion itself changes radiologically, or in rare instances may have a second type of vascular anomaly develop in close proximity) but this is uncommon and it is therefore thought that most venous angiomas do not undergo any significant change at all. Most venous angiomas occur alone, while some are associated with other vascular malformations such as cavernous hemangiomas. Some venous angiomas occur in multiple sets within the brain (i.e., several of them may be found rather than just one, as in "blue rubber bleb nevus syndrome").

    4. What are the symptoms of venous angiomas?

    Alone, venous angiomas tend not to cause any symptoms. That is, the majority of venous angiomas are thought to remain dormant or silent throughout life. However, some do cause problems such as seizures or brain hemorrhage. Hemorrhage from these vessels, although very rare, can cause sudden onset of headache, associated with one or more of the following: nausea, vomiting, sleepiness ("somnolence" or "obtundation") and weakness in one or more limb(s), or some other neurological disability. They are typically not associated with chronic headaches or migraines, however, theoretically, one or more veins comprising the angioma can spontaneously "clot off" (thrombose), leading to local venous hypertension (back pressure buildup in the region's venous system) that can manifest as headache. Interestingly, if the venous angioma occurs in association with a cavernoma ( take me to the section on Cavernomas now), it is the cavernoma that usually causes a problem, and not the venous angioma.

    5. More about brain venous angioma hemorrhage.

    Hemorrhage from a venous angioma is a very rare event. It is more likely to occur if the venous angioma is associated with a cavernous hemangioma, and in such a setting, it is the cavernous hemangioma that usually bleeds, not the venous hemangioma ( take me to the section on Cavernomas now). If the venous angioma itself is thought to have bled, it is probable that one or more of abnormal-walled vein comprising the angioma ruptured. Again, this has been reported in the literature, but is rare.

    6. What are the complications of venous angiomas?

    As mentioned above, the two main complications (both relatively rare) are seizures and hemorrhage. It cannot be overstressed that most venous angiomas cause no complications whatsoever; some of course do.

    7. How are venous angiomas detected?

    Most venous angiomas are never detected unless the patient has a brain scan for another reason. This is because most venous angiomas cause no problems. They are best detected through cerebral angiography, but can also be seen in contrast-enhanced MRI scans and contrast-enhanced CAT scans, or in CT-angiography (CTA). Magnetic resonance angiography (MRA) is not a good way to look for venous angiomas because MRA looks at the arterial side of the circulation, not the venous side. Magnetic resonance venography (MRV) may pick up a venous angioma if it is not small. If there is hemorrhage associated with the venous angioma, regular (nonenhanced) CAT scans can usually detect the area of hemorrhage.

    In general, an MRI with and without contrast is an excellent way through which a venous angioma can be detected. The multiple imaging sequences used in the MRI scan can show the venous angioma along with any other vascular abnormality. CT-angiography (CT) can also be carried out as an alternative, but is not as good at picking up a commonly associated vascular malformations such as cavernous hemangioma (cavernoma) if that cavernoma is small. If a venous angioma appears "complex", it may be worth considering formal cerebral angiography to exclude the possibility of another vascular lesion such as an arteriovenous malformation (AVM; take me to the section on AVMs now).

    8. How are venous angiomas treated?

    Most neurosurgeons agree that for most persons, venous angiomas should not be directly treated (i.e., one avoids venous angioma surgery or "radiation" whenever possible). However, this should be discussed with your surgeons and physicians. If the angioma is thought to be causing seizures, one approach is to make sure there is no underlying arteriovenous malformation and, if there is not, the seizures can be treated using conventional oral anti-seizure medications such as Phenytoin (Dilantin) or another equivalent agent. If the seizures are debilitating and not controlled medically, surgery can be carried out to remove the angioma. However, the main risk of surgery is venous stroke, as such lesions are thought to drain normal brain tissue. This is something that should be discussed in detail with your physicians. It is very important that other types of blood vessel abnormalities that may exist with (e.g., cavernoma) or mimic (e.g., AVM) venous angiomas are ruled out by appropriate consultation and investigation.

    There is no effective radiation treatment (conventional or stereotactic) for venous angiomas, and as mentioned above, no treatment whatsoever is recommended for the vast majority of venous angiomas (there may be some exceptions).

    Surgery can be carried out if the venous angioma is thought to have ruptured. At the time of surgery, a previously undetected cavernous malformation or AVM may be found. In surgeries for symptomatic or enlarging cavernous malformations (cavernomas) that have an associated venous angioma (this association is common), the venous angioma is not disturbed by the neurosurgeon, but the cavernoma is removed.

    [This Message was Edited on 03/13/2007]
  2. HRgirl

    HRgirl New Member

    I have 6 of these on the left side. I have found it common in those with FMS and CFS. The MRI was done on me to rule out MS. I went to a Neurologist and he said that they couldnt tell what they were from - yet. Mine were in a non-specific part of the brain not typically seen with MS or any disease. They watch them every year to see if I get more. So far in 5 years - the same ones in the same place.
  3. karinaxx

    karinaxx New Member

    have you been checked for any vascular deseases?
    Vasculitis or Wagners Desease?
    what i got from reading about it on different sites, is that any vascular desease should be ruled out, if there are any clinical symptoms with it.

    i am also beeing checked for MS by Neurologist.

    What are your main symptoms?

  4. karinaxx

    karinaxx New Member

    From Wikipedia, the free encyclopedia
    Jump to: navigation, search
    In medicine, vasculitis (plural: vasculitides) is a group of diseases featuring inflammation of the wall of blood vessels including veins (phlebitis), arteries (arteritis) and capillaries due to leukocyte migration and resultant damage. While most vasculitides are rare, they generally affect several organ systems and can cause severe disability.

    1 Classification
    1.1 Large vessel vasculitis
    1.2 Medium vessel vasculitis
    1.3 Small vessel vasculitis
    2 Symptoms and signs
    3 Diagnosis
    4 Treatment
    5 Source
    6 External links

    [edit] Classification

    [edit] Large vessel vasculitis
    Takayasu arteritis. Primarily affects the aorta and its main branches. At least 3 out of 6 criteria yields sensitivity and specificity of 90.5 and 97.8%:

    onset < 40 years
    claudication of extremities
    decreased pulsation of one or both brachial arteries
    at least 10 mmHg systolic difference in both arms
    bruit over one or both carotid arteries or abdominal aorta
    arteriographic narrowing of aorta, its primary branches, or large arteries in upper or lower extremities
    Giant cell (temporal) arteritis. Chronic vasculitis of both large and medium vessels, primarily affecting cranial branches of the arteries arising from the aortic arch. At least 3 out of 5 criteria yields sensitivity and specificity of 95 and 91%:

    onset > 50 years
    localized headache with new onset
    jaw claudication, visual disturbances
    pain and stiffness in the neck and shoulders
    pain and/or decreased pulse of temporal artery
    ESR > 50 mm/h
    biopsy of affected artery which shows necrotizing arteritis with prominent mononuclear cells or multinucleated giant cells

    [edit] Medium vessel vasculitis
    Polyarteritis nodosa. Systemic necrotizing vasculitis and aneurysm formation affecting both medium and small arteries. If only small vessels are affected, it is called microscopic polyangiitis, although it is more associated with Wegener's granulomatosis than to classic PAN. At least 3 out of 10 criteria yields sensitivity and specificity of 82 and 87%:

    unexplained weight loss > 4 kg
    livedo reticularis
    testicular pain
    myalgias, weakness
    mononeuropathy or polyneuropathy
    new onset diastolic blood pressure > 90 mmHg
    elevated serum BUN (> 40 mg/dL) or serum creatinine (> 1.5 mg/dL)
    hepatitis B infection
    arteriographic abnormalities
    arterial biopsy showing polymorphonuclear cells
    Wegener's granulomatosis. Systemic vasculitis of medium and small arteries, including venules and arterioles. Produces granulomatous inflammation of the respiratory tracts and necrotizing, pauci-immune glomerulonephritis. Most common cause of saddle nose deformity in USA (nose flattened due to destruction of nasal septum by granulomatous inflammation). Almost all patients with WG has c-ANCA, but not vice versa. Current treatment of choice is cyclophosphamide. At least 2 out of 4 criteria yields sensitivity and specificity of 88 and 92%.

    nasal or oral inflammation (oral ulcers or purulent/bloody nasal discharge, may be painful)
    abnormal CXR showing nodules, infiltrates, cavities
    microscopic hematuria or RBC casts
    vessel biopsy shows granulomatous inflammation
    Kawasaki disease. Usually in children, it affects large, medium, and small vessels, prominently the coronary arteries. Associated with a mucocutaneous lymph node syndrome. Diagnosis requires fever lasting five days or more with at least 4 out of 5 criteria:

    bilateral conjunctival injection
    injected or fissured lips, injected pharynx, or strawberry tongue
    erythema of palms/soles, edema of hands/feet, periungual desquamation
    polymorphous rash
    cervical lymphadenopathy (at least one node > 1.5 cm)
    Isolated CNS vasculitis. Affects medium and small arteries over a diffuse CNS area, without symptomatic extracranial vessel involvement. Patients have CNS symptoms as well as cerebral vasculitis by angiography and leptomeningeal biopsy.

    [edit] Small vessel vasculitis
    Churg-Strauss arteritis. Affects medium and small vessels with vascular and extravascular granulomatosis. Classically involves arteries of lungs and skin, but may be generalized. At least 4 criteria yields sensitivity and specificity of 85 and 99.7%.

    asthma (history of wheezeing or presently wheezing)
    eosinophilia > 10% on CBC
    mononeuropathy or polyneuropathy
    migratory or transient pulmonary opacities on CXR
    paranasal sinus abnormalities
    vessel biopsy showing eosinophils in extravascular areas
    Microscopic polyarteritis/polyangiitis. Affects capillaries, venules, or arterioles. Thought to be part of a group that includes Wegeners since both are associated with ANCA and similar extrapulmonary manifestations. Patients do not usually have symptomatic or histologic respiratory involvement.

    Hypersensitivity vasculitis. Usually due to a hypersensitivity reaction to a known drug. There is presence of skin vaculitis with palpable petechiae or purpura. Biopsy of these lesions reveal inflammation of the small vessels, termed leukocytoclastic vasculitis, which is most prominent in postcapillary venules. At least 3 out of 5 criteria yields sensitivity and specificity of 71 and 84%:

    age > 16
    use of possible triggering drug in relation to symptoms
    palpable purpura
    maculopapular rash
    skin biopsy showing neutrophils around vessel
    Henoch-Schonlein purpura. Systemic vasculitis due to tissue deposition of IgA-containing immune complexes. Biopsy of lesions shows inflammation of small vessels. It is considered a form of hypersensitivity vasculitis but is distinguished by prominent deposits of IgA. This is the most common vasculitis in children. Presence of 3 or more criteria yielded sensitivity of 87% while less than 2 criteria yielded hypersensitivity vasculitis in 74%:

    palpable purpura (usually of buttocks & legs)
    bowel angina
    GI bleed
    onset < 20 years
    no new medications
    Essential cryoglobulinemic vasculitis. Most often due to hepatitic C infection, immune complexes of cryoglobulins --- proteins that consists of immunoglobulins and complement and precipitate in the cold while dissolving upon rewarming --- are deposited in walls of capillaries, venules, or arterioles. Therefore, complement will be low with histology showing vessel inflammation with immune deposits.

    Vasculitis secondary to connective tissue disorders. Usually secondary to SLE, RA, relapsing polychondritis, Behce'ts disease, and other connective tissue disorders.

    Vasculitis secondary to viral infection. Usually due to hepatitis B and C, HIV, cytomegalovirus, Epstein-Barr virus, and Parvo B19 virus.

    [edit] Symptoms and signs
    Patients usually present with systemic symptoms with single or multiorgan dysfunction. Common (and nonspecific) complaints include fatigue, weakness, fever, arthralgias, abdominal pain, hypertension, renal insufficiency, and neurologic dysfunction. The following symptoms should raise a strong suspicion of a vasculitis:

    Mononeuritis multiplex. Also known as asymmetric polyneuropathy is highly suggestive of vasculitis, since diabetes is the only other cause of this.
    Palpable purpura. If patients have this in isolation, it is most likely due to cutaneous leukocytoclastic vasculitis. If the purpura is in combination with systemic organ involvement, it is most likely to be Henoch-Schonlein purpura or microscopic polyarteritis.
    Pulmonary-Renal. Patients with hemoptysis and renal involvement are likely to have Wegener's granulomatosis, microscopic polyangiitis, or anti-GBM disease (Goodpasteur's disease).

    [edit] Diagnosis
    A detailed history is important to elicit any recent medications, any risk of hepatitis infection, or any recent diagnosis with a connective tissue disorder such as SLE. A thorough physical exam is needed as usual.

    Lab tests. Basic lab tests may include a CBC, chem-7 (look for creatinine), muscle enzyme, liver function tests, ESR, hepatitis seroloties, urinalysis, CXR, and EKG. Additional, more specific tests include:
    Antinuclear antibody (ANA) test can detect an underlying connective tissue disorder, especially SLE
    Complement levels that are low can suggest mixed cryoglobulinemia, hepatitis C infection, and SLE, but not most other vasculitides.
    Antineutrophil cytoplasmic antibody (ANCA) may highly suggest Wegener's granulomatosis, polyarteritis nodosa, Churg-Strauss syndrome, or drug-induced vasculitis, but is not diagnostic.
    Electromyography. It is useful if a systemic vasculitis is suspected and neuromuscular symptoms are present.
    Arteriography. Arteriograms are helpful in vasculitis affecting the large and medium vessels but not helpful in small vessel vasculitis. Angiograms of mesenteri or renal arteries in polyarteritis nodosa may show aneurysms, occlusions, and vascular wall abnormalities. Arteriography are not diagnostic in itself if other accessible areas for biopsy are present. However, in Takayasu's arteritis, where the aorta may be involved, it is unlikely a biopsy will be successful and angiography can be diagnostic.
    Tissue biopsy. This is the gold standard of diagnosis when biopsy is taken from the most involved area.

    [edit] Treatment
    Treatment is targeted to the underlying cause. However, most vasculitis in general are treated with steroids (e.g. methylprednisolone) because the underlying cause of the vasculitis is due to hyperactive immunological damage. Immunosuppressants such as cyclophosphamide and azathioprine may also be given.

    [edit] Source
    Jenette JC, Falk RJ. Small-vessel vasculitis. N Engl J Med 1997; 337(21):1512-23. PMID 9366584.
    Mayo Clinic on vasculitis.

    [edit] External links
    European Vasculitis Study Group
    Johns Hopkins Vasculitis Center
    Retrieved from ""
    Categories: Rheumatology | Inflammations

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  5. mezombie

    mezombie Member

    Hi Karina,

    Wie geht's in die Schweitz?

    I'm glad the weather is good. Well, at least it's a break from the heat of India! Hopefully you're not getting too much of the usual gray and rain.

    I'm sorry to read about the MRI results. I'm very brainfogged today, so I can't give much advice, but I do sympathize with having to deal with yet another abnormality.

    What caught my attention, for what it's worth, is that venous angiomas can cause seizures. An EEG could tell you whether that's the case with you. I am exploring the possibility that I may have Photosensitive Epilepsy (after much help from members of this board!) After discussing this possibility with my neurologist, I have a prescription for a sleep-deprived EEG with photostimulation to see if that's the real reason behind my so-called "vestibular migraines". It never occurred to me I might have seizures, but there are all sorts of different kinds, apparently.

    So maybe an EEG like this one might be a next step?

    Good luck, und viele Besserung fuer dich und dein Sohn.

  6. karinaxx

    karinaxx New Member

    Es ist wunderschönes Wetter hier, fast Frühling.
    Aber ich kann es kaum geniessen, zuviel Stress von allen Seiten.

    I will answer you back on this migraine thing, of cours my brain is in full swing , discovering more interesting stuff in connection with Vasculitis and Hyperactive Immune Sytem....

    will check tomorrow about your suggestion.

    hope your doing better
  7. karinaxx

    karinaxx New Member

    anybody, your thoughts..........

  8. mymichelina

    mymichelina New Member

    I had an MRI that showed white matter lesions in the pons and mid-brain area so they ruled out multiple sclerosis and said they were likely caused by Microvascular Disease. I don't really know what to think of mine either.
  9. Crispangel66

    Crispangel66 New Member

    After my brother got one he started having seizures and still has them today. I hope you don't go through the same thing. Good luck.
  10. karinaxx

    karinaxx New Member

    i was either busy or to exhausted and in pain from beeing to buisy.

    So here it is: I was at the Neurologist yesterday. First time that I had the feeling I am in fairly combatant hands.
    There were two of them and both were very interested and both want to shed some light on the symptoms I have. Both of them were a bit puzzled and made some remarks to the MRI being slightly off, but no concrete answers. They want me to come in for 5 days to the Hospital and they will investigate the whole range of CNS, Vascular, MS (Lumbar Puncture) Diseases.
    I am very happy about that, at least it is taken serious and I hope I get some answers and getting treatment options ??!! Though, I am hesitant, since I know that the CFIDS diagnosis done two years ago is correct. I did not tell them about my son, will do that , when I do have the investigation done!

    In the meantime I will see Dr.Meirleir in a few days and I hope to get some answers for my son.

    When I asked them about the Venous Angioma, they said, that being in the region where I have it, it will and can not cause the symptoms I have.

    I am sceptical, but did not answer anything back on this. They are the experts and so be it.

    All what I said is, that I would like to be checked for Wagener D. , which is a Vascular Disease, and she again said , that Wagener does not show up in my MRI, whatever that means, but she did take it serious, since my symptoms like Sinuses and Asthma (problems with breathing), kidney problems, could point to it.


    I can not give you any answers, since I do not know much about Vascular Diseases. Purpura is one of them and like all this stuff is, I think, a problems of a Hyperactive Immune System (Autoimmune due to to high viral loads and a disfunction of a part of the CNS ?) and I just confirms the theory I have , that ME/CFIDS could be a Neurological Autoimmune thing and they come as you know often in clusters in the same person or family.
    Did you not get the treatment option when you was diagnosed with Purpura? I think it is Cortisone , but I suggest you Google Vascular Diseases and Wikipedia also has some information on it.

    To all others, I don’t know more than you do, wish I would and could be of more help.

    Thanks for all your answers
    Take care

    [This Message was Edited on 03/16/2007]
  11. karinaxx

    karinaxx New Member

  12. victoria

    victoria New Member

    I don't know whether to say great they found something at least, or not... but please keep us posted as to what DeMerlier says and what you find out?

    all the best,
  13. karinaxx

    karinaxx New Member

    i am just glad that they are checking me for everything and taking it serious, whatever they find.
    thanks for your good wishes and yes, i will keep you all updated on Meirleirs visit.
    i am hoping for some good advice and treatment options for my son!

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