This is the fifth essay in my series of why Hillary Clinton has brain damage. I was still trying how to figure this out--the best way to present often highly technical information to a lay audience (although I know that there are other physicians here). In some essays I presented in the text relatively little cut-and-paste from journal articles, although I did link to them. In other essays I presented text extensively from cited journal articles. This was especially true in essay number 4 about PCS. In that essay, I particularly presented lots of text because PCS is such a controversial subject, so that lots of explanatory material was needed. From the comments received to the essays (for most of which I am grateful), it was apparent that there was still considerable misunderstanding of the material. This material requires close reading to be correctly understood.

Today's essay is about cerebral dural sinus thrombosis (DST), which actually is a much simpler situation that the controversial PCS situation. To really understand DST, you must have some understanding about the cerebral venous circulation. More on that below.

Bias alert: I do not like Hillary Clinton. All the material linked in this essay are from peer-reviewed medical articles. Where there is speculation, and I certainly admit to speculation, I will try to be certain the readers understand which is speculative. This whole series of essays would be unnecessary if Hillary released her unaltered medical records for independent medical analysis.

I have and continue to request the dissemination of my essays by those who feel the inquiry is worth that effort. I am not afraid of FACTUAL criticism. I am hopeful that those physicians amongst us contribute to commentary--or even write independent essays of their own regarding my material.

Because the subject matter is DST, I will usually only cite limited portions of the linked articles. At the end of this essay, I will translate, in a very simplified fashion, from Medical to English.

Undebated and uncontested is the FACT that HRC suffered from a DST. What we don't know, amongst many other things, is how much more symptomatic she became after the DST. We don't know if Clinton sustained a venous infarction nor subarachnoid hemorrhage as a result of the DST. I will posit that, contrary to the MSM's mindless HillBot talking, that those sequelae have been much more detrimental than stated.

The conventional wisdom (?) about these two events, concussion (aka mTBI) and DST is that the mTBI occurred about 2 weeks before the DST was diagnosed. Since DST has an incidence of between 2.7 and 7 per million, this situation is often over-looked. Which came first: the chicken or the egg? In this case, the comparison would be the mTBI or the DST. The timing of such events may actually be more deleterious if the DST preceded the mTBI as opposed to the more widely believed reverse situation. More on this in next essay.

Both conditions are well-known causes of neuropathology (in people talk this means "brain damage"). The questions before us is how much? Not included in this article are the following:
1. Hillary's Sociopathy
2. Hillary's politics
3. Consideration of the presence of subcortical vascular dementia (SVD) also known as Binswanger's disease; the reference to which is in a possibly faked medical document from Dr. Bardack.

The above illustration is, of course the topic of interest, taken from the article Cerebral and sinus vein thrombosis. The lateral sinus is also known as the transverse sinus. Sometimes the whole complex from the superior sagittal sinus (SSS) to the origin of the jugular vein (which is the continuation of the sigmoid sinus at the skull base) is called the "sigmoid sinus" because of it's resemblance to the letter S.

More basics: thrombosis means blood clot. Blood clots age along a continuum from acute to sub-acute to chronic. The difference is somewhat arbitrary according to cut-off points, because the occurrence and maturation (which is usually dissolution) of blood clots continues smoothly over a time frame particular to the victim. When blood clots (thromboses) do not complete dissolve, they are said to be "recanalyzed", which means that blood is now flowing through a portion of the vein previously obstructed by clot. In the majority of cases, a completely obstructed blood vessel, even arteries, are only partially recanalyzed.

What are the presenting signs of of DST?

With such a wide spectrum of neurological signs and mode of onset the clinical presentation of CVT is mainly divided into the five following patterns:
1. Isolated Intracranial Hypertension
2. Focal Cerebral Signs
3. Cavernous Sinus Thrombosis
4. Subacute Encephalopathy
5. Unusual Presentations

What are some the consequences of DST? These are some of the complications--

http://www.ncbi.nlm.nih.gov/pubmed/17183989
Complications associated with cerebral venous thrombosis.

Residual epilepsy

Seizures are observed only in patients who had seizures and focal signs in the acute stage, and only in a minority. It has been reported in 10% to 30% of patients who had seizures during the acute stage. Out of a follow up of 77 patients, 4 had residual epilepsy in Preter et al. analysis while 7 out of 57 patients suffered recurrences in a French study. (3
Seizures usually occur in the first year and are easily controlled with antiepileptic drugs. Preter et al. recommend that due to low occurrence of seizures it is appropriate to maintain anticonvulsant therapy for a year and to taper off gradually thereafter. If seizures recur, anticonvulsants should be given on a long-term basis.
Psychiatric complications

Psychiatric complications are rare and depend upon the area of involvement. There can be an acute presentation like Korsakoff-like amnestic syndrome with confabulation in bilateral mesial temporal lobe infarction following bilateral cavernous sinus thrombosis or there may be long-term deterioration in behavioral and cognitive functioning. Data on this subject is extremely varied with a Dutch study group stating cognitive impairment in 35% of their patients while a Portugal study group argues that cognitive impairment is not that frequent. However, both acknowledge that despite the functional recovery, more than half of the patients still feel unwell depressive and anxiety symptoms.

Interesting cases of catatonia and dementia syndrome are described in separate case reports, making CVST a constant headache for researchers and physicians.

Other rare long-term complications

Other rare long-term complications like progressive diskinesia, spasmodic torticollis with multiple cranial involvements, visual impairment and other residual neurologic deficits are reported in different parts of the world. It is interesting that there is no significant effect of treatment on these long-term outcomes.

Seizures with symptomatic DST may not be so rare as many in the press and c99 have conjectured. Early seizures with symptomatic DST

Early seizures in cerebral vein and dural sinus thrombosis: risk factors and role of antiepileptics.

Prospective, multinational, observational study that included 624 consecutive adult patients with symptomatic CVT who were diagnosed at 89 participating centers in 21 countries from May 1998 to May 2001.

Frequency of Presenting and Early Seizures

Two hundred forty-five patients (39.3%) experienced presenting seizures before the diagnosis of CVT. Seizures were focal in 58 (9.3%) patients, generalized (from onset or secondarily) in 123 (19.7%), or of both types in 64 (10.3%). Three (0.5%) patients presented with convulsive status epilepticus…Twenty-six (60.0%) of the 43 early seizures were recurrent, as they were experienced by patients who already had a presenting seizure.
In logistic-regression analysis, supratentorial parenchymal lesion on admission CT/MR (OR 3.09, 95% CI 1.56 to 9.62) and presenting seizure (OR 1.74, 95% CI 0.90 to 3.37) predicted new early seizures.

Weakness of this study: In fact, we did not register familial history of
seizures and we did not record electroencephalographic data.

Despite the study authors not performing their own electroencephalography, does not mean the results are false; it does mean the authors relied upon other medical experts for the diagnosis of epilepsy. This was a huge, international study, which would have criteria to be satisfied before allowing patient entry into the study.

What is the mechanism of neuronal injury in DST?

Infarctions and haemorrhage

Infarctions and haemorrhage are endpoints of CVT [cerebral venous thrombosis] cascade. These are most important determinants of neuronal injury and long term outcome of patients. Haemorrhagic tendency in venous thrombosis is more frequent as contrary to arterial thrombosis, occurring approximately in 10-50% of cases. Haemorrhagic infarctions principally affect the cortex and gray-white matter junction. The bleeding in CVT is attributable to increased venous and capillary pressure. Small cortical veins are vulnerable to rupture in the setting of these haemodynamic changes, resulting in bleeding on the cortical surface. Sudden development of venous occlusion due to thrombus, rather [than] slow developing occlusion is presumably responsible for the haemorrhagic infarction.
Neurological recovery or long term outcome is dependent on extent of neuronal injury and early recanalization of occluded sinuses.

A large international study published on a subset of patients with intracerebral hemorrhage, especially Early-Intracerebral Hemorrhage (E-ICH) about predictors of outcome in DST.

This study was conducted in the largest prospective cohort ever published of CVT patients. It has shown that: (1) the proportion of CVT revealed by ICH is high; (2) among CVT patients, those with E-ICH were older, and more likely to have a severe clinical presentation and a worse 6-month outcome that CVT patients without ICH; (3) in patients with E-ICH, independent predictors of death or dependency were older age, male gender, having a thrombosis of the deep cerebral venous system or of the right lateral sinus, and having a motor deficit; (4) in patients with D-ICH, those who had a worse outcome were less likely to have been treated by heparin, and to have had an E-ICH.

Did Hillary have E-ICH? Only her doctors know and they ain't telling'.

More on this ICH theme. One form of ICH is subarachnoid hemorrhage (SAH) which is a usually diffuse bleed between the arachnoid membrane and the brain itself (including the pia mater, usually). Here's another quote about acute SAH as initial presentation of dural sinus thrombosis:

The spectrum of clinical presentations of CVT ranges from headache with papilledema to focal deficit, seizures and coma. Up to 75% of cases are characterized by focal neurologic deficit and headache; 30-50% of affected patients present with seizures, often followed by Todd's paresis. Rare, but classical, clinical pictures are those of SSS thrombosis (4%) with bilateral or alternating deficits and/ seizures. SAH is related to ruptured aneurysm in 85% of cases and to nonaneurysmal perimesencephalic hemorrhage in 10%; the remaining 5% are related to a variety of rare conditions such as arterial dissection, dural arteriovenous fistula, pituitary apoplexy, and cocaine abuse. In an exhaustive review of SAH, CVT was not listed as a cause of SAH. This omission is rather surprising because erythrocytes are commonly present in the CSF of patients with CVT. One can speculate that plain CT scan may cause small amounts of subarachnoid blood to be overlooked, especially when the blood is located in the sulci of cerebral convexity or when larger amounts of extravasated blood are present in the sub acute stages. The exact cause of SAH associated with CVT is unknown. Venous hemorrhagic infarct can be responsible for secondary rupture into subarachnoid space and cause SAH. None of the patients reported herein had intraparenchymal signs of bleeding on CT scan or gradient recalled echo (GRE) MRI. DST with secondary venous hypertension may lead to SAH into the subarachnoid space due to rupture of fragile, thin-walled cortical veins. Sinus thrombosis may produce dilatation of the cortical veins, which may rupture and bleed into the subarachnoid space and produce an SAH. A similar mechanism has been proposed to explain the presence of extravasated blood confined to the prepontine or interpeduncular cistern in nonaneurysmal perimesencephalic hemorrhage.

Please note that MRI is about 6-10 times more proficient at detecting SAH than is CT.

Hillary Clinton had a right lateral sinus thrombosis. Right lateral sinus is a bad prognostic indicator

Four main clinical patterns of CVT are generally recognized and these include presentation with focal neurological deficits and/or seizures, isolated intracranial hyper-tension, subacute diffuse encephalopathy and painful ophthalmoplegia and the distinction of patients into these clinical patterns carries prognostic implication. Altered mental status and cerebral haemorrhage at presentation have been found to be the most consistent and strongest predictors of death and disability. Older age (>37 years in ISCVT), male sex, seizures at admission, rapid evolution of thrombosis, the presence of focal deficits and CNS infection and cancer as the underlying cause also predict poor outcome. Although the site of thrombosis has not been found to correlate with the outcome in certain studies, ISCVT found involvement of cortical veins, deep cerebral veins and superior sagittal sinus, intracerebral haemorrhage on right side…to be poor prognostic factors. It is generally recognized that although several predictors of good and bad outcome have been identified in patients with CVT, the prognosis of a given individual patient remains variable and highly unpredictable.

Few studies have looked at the long-term outcome in patients with CVT. One of the common sequelae in these patients is epileptic seizures. These almost always occur in those patients who had seizures during the acute stage of the disease and a rate of 5-16% has been reported in various studies. Studies using various neuropsychological batteries aimed at assessing long-term cognitive outcome have reported cognitive impairment in approximately 35% of the patients in different cohorts usually in the form of non-fluent aphasia, working memory deficits and depression.

Increasing age, male gender, having a thrombosis of the deep cerebral venous system, having a motor deficit, and having a right lateral sinus thrombosis are predictors of poor outcome in CVT patients with ICH

More on prognosis: DST prognosis in 59 patients

Results
Between July 1992 and November 1996 60 patients were recruited in 14 hospitals in The Netherlands and the United Kingdom. No patients were lost to follow up. One patient was ineligible due to a wrong diagnosis (arterial cerebral infarction). Thus 59 patients (50 women, nine men) were studied. Mean age was 37 years, with a range from 18 to 80 years (median 33 years).
After 12 weeks six patients had died, and four patients had an Oxford handicap score of 3 or more, which results in 10 of the 59 patients (17%) with a poor outcome. All patients at entry without intracerebral haemorrhage, and who were not in coma (GCS(39%) had some degree of impaired conscious- ness. Twelve patients (20%) presented with a clinical syndrome of isolated intracranial hypertension (headache with or without papilloedema or visual impairment, and no other symptoms and signs).
The mean delay between the onset of symp- toms and the time of randomisation at admission was 10.6 days (range 1 to 30 days, median 8 days). Five patients (9%) had an acute onset, with symptoms developing within 48 hours before the diagnosis. There were no patients with progression over more than a month.

This what DST with ICH looks like Note, these are scans from 4 different patients. Source: Isolated Lateral Sinus thrombosis.

Long-term prognosis in 77 patients with DST

Results Sixty-six of 77 patients (85.7%) had no neurological sequelae during follow-up. Eleven patients (14.3%) remained neurologically impaired. Two who initially presented with isolated intracranial hypertension had blindness due to optic atrophy. The other 9 had focal signs at the time of CVT and were left with various cognitive or focal deficits. Four of 28 (14.3%) patients who had seizures at the acute stage had recurrent seizures. One of the 51 patients with lateral sinus thrombosis developed a dural arteriovenous fistula. Nine of the 77 patients (11.7%) suffered a second CVT, all but one in the first year. Noncerebral thrombotic events occurred in 11 patients (14.3%). No recurrence of CVT occurred during later pregnancies, but 1 patient had a postpartum deep vein thrombosis.

Conclusions In the present series, CVT has an essentially good long-term prognosis. The frequency of long-standing epilepsy was low, suggesting that long-term anticonvulsant treatment is not necessary in the majority of cases. A second CVT or another thrombotic episode occurred in 20% of patients, stressing the need in a minority of cases for long-term anticoagulation.

Now for a very oversimplified analogy for those of you not fluent in "Medical". Imagine an automobile with dual exhausts--but each of the exhausts arises from one primary outlet, then splits in two. The "exhaust" in this case is venous blood leaving the brain. Then imagine someone stuffing a potato into one of the exhaust pipes (nasty trick, eh). So where does the exhaust go? If the other exhaust is wide open, then--no problem. But what happens if the other exhaust is partially or completely obstructed? Yes, back pressure is transmitted to the engine--not good. In the case of this analogy, the "engine" is the brain. Back-pressure first manifests itself by dilating the capacitance vessels, i.e., the dural sinuses. When dilation of these sinuses is no longer able to contain the back-up exhaust, i.e., blood, then smaller veins are distended. Small veins do not have adequate capacity to compensate very well from the back-pressure--so they burst. When the veins pop, the bleeding may go into one or two or three of the following places:
1. into the substance of the brain (ICH)
2. into the subarachnoid space (SAH)
3. in a space between the arachnoid and the dura--the dura being the membrane through which the majority of brain venous drainage flows. This is known as a sub-dural hematoma (SDH).

None of these outcomes are particularly pleasing.

As mentioned above, there's lots of speculation here.

Let me reiterate some important issues that need elucidation:
1. What was Hillary's state of consciousness at symptom onset?
2. Did she present with seizures?
3. Did she present with focal neurological deficits?
4. What did her initial imaging reveal, such as a bleed or a stroke?
5. Was the DST really acute or did it actually precede the mTBI.
6. What does her EEG show?
7. What do her neuropsychologic tests show?

I will continue to speculate. The incompetence due to brain damage is a much more serious issue than her corporatist, war-mongering, sociopathic traits.

Please, feel free to disseminate these 5 essays as you see fit. I tolerate Factually-based criticism--but please, not Wikipedia. Your comments are welcome--if factual. By the way, some comments about the 4th essay were at variance with my knowledge and experience; but, I elected to not deflect onto subjects having only peripheral bearing on the main subject matter.