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ERMudPhud

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So here is a case I saw over the weekend. Lets see what you all think.

CC: Worst headache of life

HPI: 27 year old female G4P4 7 days postpartum from a c-section under epidural anesthesia for poor progression of labor presents with worst headache of her life associated with N/V and severe photophobia. She states that the headache began suddenly at 6/10 around 9:00 p.m and then increased to its current 10/10 in 10-15 minutes. She describes it as frontal radiating to occiput and "like my head is going to expode." She took two percocet she had left from her postop meds and fell asleep but when the percs wore off the pain was as intense as ever. She has a migraine history with typical migraines characterized by frontal pain with N/V, photophobia, and scotoma but her migraines always respond to Excedrin migraine formula and she has never visited an ED for them. This headache is more intense and more global than her migraines and does not have any associated scotoma. She has had no fevers or chills. no rashes, no seizures, no neuro defecits.

PE: RR=24 HR=108 BP=160/110 afebrile normal sat
Gen: Young woman in a dark room curled into fetal position crying
HEENT: NC/AT PERRL 4mm TM's-clear fundi-cant be visualized secondary to photophobia
Neck: no meningismus no bruits
Chest/cor;normal except for slight tachycardia
Abd: NT incision CDI
extr: no edema
Neuro: A&Ox3 completely nonfocal DTR's brisk and symmetric but without clonus, toes down going. except could not really measure visual acuity do to severe photophobia

Workup
Urine: no protein
CBC,LFT's-normal
CT head without contrast-normal
LP- Opening pressure=21cm, normal glucose,protein, no cells, no xanthochromia

ED course: no real improvement with compazine and Benadryl. Sleeping with lots of Diluadid and Zofran but still in pain. With pain control BP down to 130/80 and HR down to 80 RR down to 16


So I ordered an MRI/MRV

First question: what was I looking for on the the MR

Second question: What else should be on your differential and I'll send a stuffed zebra to the first person who includes the eventual diagnosis on their differential
 
ERMudPhud said:
So here is a case I saw over the weekend. Lets see what you all think.

CC: Worst headache of life

HPI: 27 year old female G4P4 7 days postpartum from a c-section under epidural anesthesia for poor progression of labor presents with worst headache of her life associated with N/V and severe photophobia. She states that the headache began suddenly at 6/10 around 9:00 p.m and then increased to its current 10/10 in 10-15 minutes. She describes it as frontal radiating to occiput and "like my head is going to expode." She took two percocet she had left from her postop meds and fell asleep but when the percs wore off the pain was as intense as ever. She has a migraine history with typical migraines characterized by frontal pain with N/V, photophobia, and scotoma but her migraines always respond to Excedrin migraine formula and she has never visited an ED for them. This headache is more intense and more global than her migraines and does not have any associated scotoma. She has had no fevers or chills. no rashes, no seizures, no neuro defecits.

PE: RR=24 HR=108 BP=160/110 afebrile normal sat
Gen: Young woman in a dark room curled into fetal position crying
HEENT: NC/AT PERRL 4mm TM's-clear fundi-cant be visualized secondary to photophobia
Neck: no meningismus no bruits
Chest/cor;normal except for slight tachycardia
Abd: NT incision CDI
extr: no edema
Neuro: A&Ox3 completely nonfocal DTR's brisk and symmetric but without clonus, toes down going. except could not really measure visual acuity do to severe photophobia

Workup
Urine: no protein
CBC,LFT's-normal
CT head without contrast-normal
LP- Opening pressure=21cm, normal glucose,protein, no cells, no xanthochromia

ED course: no real improvement with compazine and Benadryl. Sleeping with lots of Diluadid and Zofran but still in pain. With pain control BP down to 130/80 and HR down to 80 RR down to 16


So I ordered an MRI/MRV

First question: what was I looking for on the the MR

Second question: What else should be on your differential and I'll send a stuffed zebra to the first person who includes the eventual diagnosis on their differential
Click to expand...

SAH

and with my zebra rifle, i shoot a bullet marked for "Sheehan's postpartum necrosis" :laugh: not really any signs or symptoms of it (except for maybe the optic symptoms) but hey, you said it was a zebra, right? 😀
 
Did you say a stuffed Zebra!??????

Well.......hmmmm....MRI to r/o venous sinus thrombosis and other vascular/parenchymal structural causes (tumor, brain abscess, arteriovenous malformation).

Order: Thyroid Panel.

Hold for obs

R/O PPD.


mmmmmm zebra mmmmmmmmmmmmmm :laugh:
 
So it's most likely vascular given the abrupt onset.

- SAH seems to have been ruled out by absence of xanthochromia,
- cavernous sinus thrombosis is a possibility, but not likely
- trigeminal neuralgia, not the typical presentation but possible
- giant cell arteritis
- cluster headache syndrome, not typical as this patient didn't have lacrimation
- carotid, vertebral, or other artery dissection
- AVM
- ischemic stroke (some ischemic strokes do cause pain in individuals)
- drug induced (e.g., cocaine) or drug withdrawal
- Arnold-Chiari malformation (more common than one thinks)

I'm fresh out of ideas...
 
Aneurysm, Preeclampsia, cavernous sinus thrombosis.
 
Good case.

I"m going to have to place my vote for dural sinus thrombosis. Slightly elevated opening pressure goes with that. Cavernous sinus less likely, as that's generally secondary to sinus infection and the symptoms are typically unilateral. Maybe sagittal sinus or transverse sinus thrombosis?

Too far out for post-spinal headache, though something to think about. Opening pressure a bit low to clinch a dx of pseudotumor. AVM possible, but less likely since sudden onset would indicate a rupture that should be seen on CT or found in the CSF. BP and normal urine argue against pre-eclampsia. Sheehan's doesn't generally present with acute onset of headache, does it?
 
Sessamoid said:
Good case.

I"m going to have to place my vote for dural sinus thrombosis. Slightly elevated opening pressure goes with that. Cavernous sinus less likely, as that's generally secondary to sinus infection and the symptoms are typically unilateral. Maybe sagittal sinus or transverse sinus thrombosis?

Too far out for post-spinal headache, though something to think about. Opening pressure a bit low to clinch a dx of pseudotumor. AVM possible, but less likely since sudden onset would indicate a rupture that should be seen on CT or found in the CSF. BP and normal urine argue against pre-eclampsia. Sheehan's doesn't generally present with acute onset of headache, does it?
Click to expand...

Ack! I meant dural sinus thrombosis on my post, not CST, tsk tsk, my bad.

So what's the answer?

Q
 
Um, yeah . . . I meant dural sinus too . . . or whatever the right answer is.
 
Nobody has got it yet and if you are like me you've never heard of it but I may invite our friends from Neuro, OB/Gyn, and Rads in to play.
 
I suck at neuro. (Kinetic motto: if it's above the neck or below the pelvis, it doesn't exist.) I'll just say pseudotumor cerebri. Whatever. It's not even a zebra. Woo.
 
slight hint: The diagnosis was eventually made by the radiologist who I also believe had never actually seen a case.

Second weak hint: shortly after the MRI the patient had a T/C seizure

So far nobody has got it.
 
Amniotic fluid embolism
 
pneumocranium (from when the Gas R-1 squeezed that air filled syringe a little too much).

C
 
OK, I'm sticking with postpartum cerebral vein thrombosis secondary to epiudural. But would also consider postpartum eclampsia.

well.........................
 
You will NOT believe this, but, two nights ago, we had almost the EXACT same case at our ED - but we didn't have the answer before I went home, and I didn't follow up tonight.

Postpartum 5 days, s/p epidural, NSVD, hypertensive 160/100, Headache "worst of her life", Indian female, but in US for years, HA worse when supine, better when upright, no protein in urine, no edema.

Epidural abscess.
 
Apollyon said:
Epidural abscess.
Click to expand...

It's a good thought, but I doubt the right answer (only because it's not a zebra). Looks like none of us are lucky OR good.
 
kinetic said:
It's a good thought, but I doubt the right answer (only because it's not a zebra). Looks like none of us are lucky OR good.
Click to expand...

My luck was this weekend when I didn't burn my manhood when the burger splattered. Then I punctured my nondominant thumb with a blunt object - got a purty lookin' weird wound now.
 
Brief review of Apollyon's post:

Status: lucky

Procedure: s/p hot oil on pants, manhood intact

Complications: blunt object injury to thumb

Prognosis: Negative
 
GrandPa! said:
OK, I'm sticking with postpartum cerebral vein thrombosis secondary to epiudural. But would also consider postpartum eclampsia.

well.........................
Click to expand...
Cerebral vein (or "dural vein") thrombosis post-partum isn't related to epidural anesthesia, but rather to the hypercoagulable state of pregnancy. It's pretty rare, but not so that it's reportable. The first case was reported long before the use of epidural anesthesia (or even the advent of general anesthesia, IIRC).
 
ERMudPhud said:
Nobody has got it yet and if you are like me you've never heard of it but I may invite our friends from Neuro, OB/Gyn, and Rads in to play.
Click to expand...
If you'd never even heard of it, then I doubt it's likely any of us are gonna get it. I still think dural vein thrombosis (edited to replace "abscess", which wasn't at all what I was meaning) has to be foremost on the differential with the information you've given us.
 
Some questions. Was the pregnancy normal (ie full term, any complications)?

MRI/MRV looking for venous sinus thrombosis and acute infarct.

Also, what does the pituitary look like on the MRI?

I'd like to throw in a zebra: lymphocytic hypophysitis.

Was there a post partum ultrasound done (just curious)?
 
Possibles :
Arnold Chiari Malformation
Arachnoiditis
SDH
Accidental puncture of the dura
HELLP

That's all I can think of really. I'd like to know what it actually was!
 
I don't post often, but I couldn't resist...

Tolosa Hunt Syndrome --
Often confused with Cavernous Venous Thrombosis.
To be fair, it is often, but not always, associated with oculomotor palsies.
A stuffed zebra would complete my little girl's extensive stuffed animal collection...
 
I was thinking amniotic fluid embolism at first but I think I'll go with cerebral vein thrombosis (there by ensuring that it will be nither). Since it's niether I'll then go with AMI with GI Bleed or malingering which are my two recent faves.

BTW if ERMudPhud comes back with "Oh, I don't know what it was. I was hoping you guys did." We'll all meet up at the Denver airport and plan our retaliation. 😀
 
I just saw your cross-post on the radiology forum.

How about RPL or PRES (the other name for it)? aka Reversible posterior leukoencephalopathy or the posterior reversible encephalopathy syndrome.

Other differentials: Now that the presence of blood and WBC's in CSF is ruled out, other possibilities are dural sinus thrombosis, Sheehan's, and lymphocytic hypophysitis. A severe CSF leak with acute intracranial hypotension may also give some, but not all of the Sx you mentioned.
 
Sessamoid said:
Cerebral vein (or "dural vein") thrombosis post-partum isn't related to epidural anesthesia, but rather to the hypercoagulable state of pregnancy. It's pretty rare, but not so that it's reportable. The first case was reported long before the use of epidural anesthesia (or even the advent of general anesthesia, IIRC).
Click to expand...


I agree that a hypercoagulable state of pregnancy ( or from oral contraceptives) is a predisposing factor but epi's without dural puncture have been reported. CVT was the cause.
ref 1
ref 2

OK............. What was the rad dx?................c'mon we're dyin'

:laugh:
 
I haven't forgotten about you all. I am currently in discussions with one person who may have gotten pretty darn close. I'll post the answer this evening. Remember you are looking for something that would show up on MR but not on a noncontrast CT and would give you a normal LP except for a slight increase in opening pressure.

In answer to Voxel's questions she had an uncomplicated pregnancy and the c-section was done for failure to progress in labor. I do not believe their had been a postpartum ultrasound yet. The MR venogram was normal and the sella was normal as well
 
Docxter said:
I just saw your cross-post on the radiology forum.

How about RPL or PRES (the other name for it)? aka Reversible posterior leukoencephalopathy or the posterior reversible encephalopathy syndrome.

Other differentials: Now that the presence of blood and WBC's in CSF is ruled out, other possibilities are dural sinus thrombosis, Sheehan's, and lymphocytic hypophysitis. A severe CSF leak with acute intracranial hypotension may also give some, but not all of the Sx you mentioned.
Click to expand...

You can see PRES on noncontrast CT - we saw it last week (this is good stuff!).
 
Getting desperate...

Retrobulbar hematoma?
Echinococcus? (T/C seizure)
 
Is this Sheehan's syndrome with possible reperfusion injury? I don't know. On MR you would be looking for a hemorrhagic lesion in the pituitary.

I don't even know if this is possible, but I took a shot at it.
 
Oh the pressure of not knowing......
OK.... now we're stretching....

1. r/o idiopathic intracranial hypertension (pseudotumor cerebri)

2. r/o reversible cortical lesions in the territory of the posterior cerebral artery sec to PPE

better just go out and buy a zebra.


🙁
 
Apollyon said:
You can see PRES on noncontrast CT - we saw it last week (this is good stuff!).
Click to expand...

Actually, often you can't see it on CT and it's only seen on MRI.
 
ERMudPhud said:
The MR venogram was normal and the sella was normal as well
Click to expand...

Not to be a pain, but I just wanted to point out that the usual technique of doing MRV is called time-of-flight. It can miss a small percentage of dural venous thromboses. In those cases, a direct catheter angiogram, MRV with phase-contrast technique, or possibly a CTV would be helpful (though the last one is not adequately investigated for this indication). But it is a very good screening study and should be done first, since the other ones have their own deficiencies as well. Most of the times though, you don't need an MRV to diagnose venous sinus thrombosis and just a plain MR is sufficient to rule it in.
 
cavernous angioma
capillary telangiectasia
 
ERMudPhud said:
slight hint: The diagnosis was eventually made by the radiologist who I also believe had never actually seen a case.

Second weak hint: shortly after the MRI the patient had a T/C seizure

So far nobody has got it.
Click to expand...

Well, until you posted this, I was going to express surprise that nobody has included plain vanilla "migraine" in their list.
I guess now I'll go with amniotic fluid embolism. I've never seen it either.
 
The MRV is for cerebral venous sinus thrombosis, which is a good thing to look for.

I think posterior leuckoencephalopathy is an excellent suggestion. I would place my money on this. I've lost count of the number I've seen in the preggies.

Migraine is an obvious thing that should be on the diagnsosis, although it sounds like this is not a normal HA for the pt.

zebras: retroclival hemorrhage (especially if your CT and LP were negative), Sheehan's (which can range from almost asymptomatic to catastrophic adrenal crisis..), Call-Fleming syndrome. There is also something called perimesencephalic hemorrhage that is basically benign, thought to be a venous bleed.

I have now officially scraped the bottom of my all too small neuro barrel.
 
Old MD said:
There is also something called perimesencephalic hemorrhage that is basically benign, thought to be a venous bleed.
Click to expand...

Nonaneurysmal perimesencephalic subarachnoid hemorrhage (NAPSAH) would have been a good choice except the LP had no RBCs and no xanthochromia and also there was no "perimesencephalic hemorrhage" on the CT.
 
So here is a summary of the MRI report

Imaging: sagittal T1 weighted, Axial FLAIR, diffusion weighted, and gradient echo scans. MRV by 2D time-of flight. No gadolinium secondary to nursing

FLAIR images: multiple areas of high signal primarily in posterior frontal cortex and posterior parietal/occiptal cortex

Diffusion images: high signal in some areas of frontal regions

ADC map may show decreased signal in left frontal region

MRV is unremarkable

Gradient echo- no occult hemorrhage

Impression: Multiple areas of abnormal signal intensity primarily involving the gray matter of bilateral frontal convexities and posterior occipital lobes. Findings suggestive of Postpartum Cerebral Angiopathy or Posterior Reversible Leukoencephalopathy.

The presumed diagnosis on admission was Postpartum Cerebral Angiopathy. Even after spending the last two days reading about these diseases I still can't define the difference between them very clearly. In many ways they fall within a continuum of related syndromes that also includes some of cerebrovascular effects of eclampsia. Call-Fleming which was also mentioned seems to be quite similar as well. I'll let Docxter post the PM he sent me which helped define the difference between Postpartum Cerebral Angiopathy and PRES for me. I'll also let Docxter and the other Rads people discuss the specific findings and how they fit or don't fit with PCA or PRES. As of today we still didn't have an angiogram but at least she still has no neuro defecits and hasn't seized again. An EEG did show abnormalities in the frontal lobes.

From the point of view of better to be lucky than good. I had a patient on whom I did more than my average workup. I average only ordering an MR for about every 40 shifts I work and >80% have shown significant emergent pathology. I ended up finding a disease that I hadn't even heard of and which has significant morbidity. Case reports of significant hemorrhage, stroke, and death from PCA exist. In a patient with a migraine history and a somewhat migraine like HA I might have stopped after the CT and LP. Only the fact that she wasn't a complainer (never been to the ER) and an opening pressure a little higher than I would have liked pushed me to order the MR. Even then I wasn't looking for what I found. Sort of makes me wish the metal detector in Triage doubled as whole body MRI scanner.

So, I think Docxter probably deserves a stuffed zebra. I can probably find one for anyone else who thinks they deserve one too.
 
ERmudPhud:

Great case!

I thought of PRL, because it is very common, I think it is seriously underdiagnosed. whenevr a preggie has a neuro problem it is up there on the differential for me, with hellp etc. I have seen it about 15 times. As you said, it would not have been picked up if you didn?t order the MRI, and I think that?s one reason many cases go undiagnosed.
Docxter made a good call there.

The funny thing is that it was described very very recently. Like within the last decade. If anyone is interested the first description is a NEJM paper by Loius Caplan et al (yeah, the big stroke guy). It?s a good read. Btw, there is a little scandalous hear say history behind it. Apparently, the resident whose name is on the author by line of that paper first saw these cases at the Brigham (where of course you see weird pregnancy related stuff because of the women?s hospital). She had been working under a mentor there who is basically regarded as the world expert on this condition (whose name I now forget). This mentor had been waiting to collect a bunch of cases before writing his paper for publication in nejm. Then the resident became a fellow at the BI (where Caplan works and had seen a few of his own cases). She then teamed up with Caplan, and scooped the Brigham guy, describing the few cases she had seen. Kind of a low blow. Caplan and co gave it their own name: PRL. It has been pointed out that PRL is actually neither ?posterior? nor ?leuko?, and when the Brigham guy finally described his huge number of cases (I think >100) in unfortunately a much smaller journal, he wrote about this as well. That paper is a VERY good one, because he describes the pathophys which he thinks is basically a HYPERPERFUSION disease ? ie. You will see it even in some patients who are not pregnant who have very high BP.

I suggested Call Fleming for a ddx, but I don?t really know much about it (maybe the neurologist here can tell us more?). I learnt it from a very bright med student (!!) from the great white north who was going into neurol. He diagnosed it before anyone else on this one case we had. All I remember is that it is something like a vasculitic picture but is not really a vasculitis. Steroids are not indicated. Bad stuff because people can go blind. It is supposed to be extremely rare.

There's all sorts of weird and wonderful stuff that we're learning about as patients get investigated more and more. However that brings up the important qustion of where to stop. I think in your patient you made the right choice becuse she was was 1. persistently symptomatic 2. the HA was different 3. the LP as you said had a higher OP.

Doxter is increased OP a sign of PRL? I don't seem to remember it being so.
 
So here are the three references that OLD MD mentioned. Call-Fleming is a reversible cerbral vasoconstriction phenomenon that sounds a lot like what was described for PCA. Interestingly a few authors have written about the vasculitis like characteristics of both Call-Fleming and PCA in terms of angiographic appearance but without any actual evidence of vasculitis. The similarity of PRES to other hyperperfusion encephalopathies like hypertensive encephalopathy, post endarterectomy encephalopathy or even high altitude cerebral edema is also interesting. I wonder if the alternating vasospasm and vasodilation seen in PCA leads to a postendarterectomy like hyperperfusion syndrome of if the vascular labillity is just a sign of the disease and not causative. It is also interesting that most cases of PCA are seen in the context of vasoactive drugs like methergine or triptans. My patient had received methergine and was also taking excedrin migrain formula which has caffeine

: N Engl J Med. 1996 Feb 22;334(8):494-500.

Comment in:
N Engl J Med. 1996 Jun 27;334(26):1743; author reply 1746.
N Engl J Med.
1996 Jun 27;334(26):1744-5; author reply 1746.
N Engl J Med. 1996 Jun
27;334(26):1745; author reply 1746.
N Engl J Med. 1996 Jun 27;334(26):1745;
author reply 1746.

A reversible posterior leukoencephalopathy syndrome.

Hinchey J, Chaves C, Appignani B, Breen J, Pao L, Wang A, Pessin MS, Lamy C, Mas
JL, Caplan LR.

Department of Neurology, New England Medical Center, Boston, MA 02111, USA.

BACKGROUND AND METHODS. In some patients who are hospitalized for acute illness,
we have noted a reversible syndrome of headache, altered mental functioning,
seizures, and loss of vision associated with findings indicating predominantly
posterior leukoencephalopathy on imaging studies. To elucidate this syndrome, we
searched the log books listing computed tomographic (CT) and magnetic resonance
imaging (MRI) studies performed at the New England Medical Center in Boston and
Hopital Sainte Anne in Paris; we found 15 such patients who were evaluated from
1988 through 1994. RESULTS. Of the 15 patients, 7 were receiving
immunosuppressive therapy after transplantation or as treatment for aplastic
anemia, 1 was receiving interferon for melanoma, 3 had eclampsia, and 4 had
acute hypertensive encephalopathy associated with renal disease (2 with lupus
nephritis, 1 with acute glomerulonephritis, and 1 with acetaminophen-induced
hepatorenal failure). Altogether, 12 patients had abrupt increases in blood
pressure, and 8 had some impairment of renal function. The clinical findings
included headaches, vomiting, confusion, seizures, cortical blindness and other
visual abnormalities, and motor signs. CT and MRI studies showed extensive
bilateral white-matter abnormalities suggestive of edema in the posterior
regions of the cerebral hemispheres, but the changes often involved other
cerebral areas, the brain stem, or the cerebellum. The patients were treated
with antihypertensive medications, and immunosuppressive therapy was withdrawn
or the dose was reduced. In all 15 patients, the neurologic deficits resolved
within two weeks. CONCLUSIONS. Reversible, predominantly posterior
leukoencephalopathy may develop in patients who have renal insufficiency or
hypertension or who are immunosuppressed. The findings on neuroimaging are
characteristic of subcortical edema without infarction.

PMID: 8559202 [PubMed - indexed for MEDLINE]



2: Neurologist. 2002 Jan;8(1):22-34.

Hyperperfusion encephalopathies: hypertensive encephalopathy and related
conditions.

Schwartz RB.

Department of Radiology, Brigham and Women's Hospital, Boston, Massachusetts,
USA. [email protected]

BACKGROUND: Hypertensive encephalopathy (HTE) is a syndrome typified by
headache, seizures, and neurologic signs associated with increased systemic
blood pressures; edema in the subcortical white matter is seen on imaging
studies and is usually reversible, although infarction or hemorrhage may
supervene. Based on previous work, we theorize that HTE is associated with
increased perfusion to the brain. Syndromes related to HTE may also be
encountered in clinical situations in which perfusion to the brain is acutely
increased without systemic hypertension (i.e., after treatment of high-grade
carotid stenoses or large intracranial arteriovenous malformations, or in high
altitude mountain sickness). We therefore refer to these conditions more
generally as hyperperfusion encephalopathies (HPE). REVIEW SUMMARY: The clinical
and radiographic data of 110 patients (average age, 50.1 years) who presented at
the Brigham and Women's Hospital with clinical and radiographic signs of HPE
were reviewed; 104 had systemic hypertension and 6 had postcarotid
endarterectomy hyperperfusion syndrome. Edema involved the subcortical white
matter and occasionally the cortex in all patients. In patients with systemic
hypertension, the edema was usually bilateral and located predominantly in the
occipital lobes; other brain regions included the parietal lobes, posterior
frontal lobes, cerebellum, and splenium of the corpus callosum. The six patients
with postcarotid endarterectomy hyperperfusion syndrome had edema in the
hemisphere ipsilateral to the operated side involving the anterior and middle
cerebral artery territories. The edema in HPE was associated with: increased low
attenuation on CT; decreased T(1) and increased T(2) signal on MR imaging;
increased cerebral perfusion on single emission computed tomography (SPECT) and
perfusion MR imaging;did not show restricted diffusion on MR imaging. The
syndrome resolved completely in most cases after the administration of
antihypertensive agents, although rarely small infarcts and hemorrhages
occurred. Three patients with thrombocytopenia developed large fatal
intracranial hemorrhages. CONCLUSION: The symptoms of HPE are usually
nonspecific, but the radiographic findings are consistent. Treatment should be
instituted rapidly and patients should be followed until the condition resolves
either clinically or radiographically; hemorrhagic complications, although rare,
can be serious.

PMID: 12803657 [PubMed]



3: Stroke. 1988 Sep;19(9):1159-70.

Reversible cerebral segmental vasoconstriction.

Call GK, Fleming MC, Sealfon S, Levine H, Kistler JP, Fisher CM.

Neurology Service, Massachusetts General Hospital, Boston.

Vasoconstriction is not recognized as a cause of cerebrovascular disease except
in the vasospasm seen following subarachnoid hemorrhage and possibly in
migraine. However, we found four patients to have transient, fully reversible
vasoconstriction and dilatation prominently involving arteries around the circle
of Willis. All four patients were evaluated for severe headaches and fluctuating
or recurring motor or sensory deficits. No cause for the clinical syndromes and
angiographic abnormalities was found. Similar patients are reported in the
literature under various nosologies. This newly recognized clinical-angiographic
syndrome should be differentiated from other known causes of vessel constriction
and dilatation; the precipitants of reversible vasoconstriction may then be
better defined.

Publication Types:
Case Reports
Review
Review of Reported Cases

PMID: 3046073 [PubMed - indexed for MEDLINE]
 
Old MD said:
ERmudPhud:


Doxter is increased OP a sign of PRL? I don't seem to remember it being so.
Click to expand...

I don't know right off the bat whether it's associated with increased pressures on LP. I have to look it up.
 
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