Health Freedom Alliance just published a story about young girls in England being bribed with shopping vouchers into getting a HPV vaccination. Now it appears one of those girls was blinded by the vaccination.

The medical report states: a 16-year-old girl who presented with near complete visual loss associated with chiasmal neuritis and a biopsy proven tumefactive demyelinating lesion on magnetic resonance imaging (MRI) in association with a recent immunization against human papilloma virus.
She had received her second vaccination against human papilloma virus 10 days prior to her presentation. There was no family history of demyelinating disease, collagen-vascular disease, or rheumatological disorders.
In the context of prior vaccination in a 16-year-old girl, acute demyelinating encephalomyelitis is likely to explain the multifocal deficits.
Larger epidemiologic studies will be needed to confirm a role of the human papilloma virus immunization and demyelinating disease.

It seems larger studies are being performed and young girls are the guinea pigs. A 16-year-old previously healthy girl presented to the
emergency room with an acute onset of visual loss over
48 hours. Initially, there was visual loss noted in the rightworsened over the next 24 hours to include visual loss
involving the left eye with a more diffuse headache. When
evaluated in the emergency room at 48 hours after onset,
her vital signs were blood pressure 116/65, pulse 68/minute,
respirations 14/minute, and temperature 98C,6 with a
completely normal general physical examination and no
signs of systemic illness. Her examination disclosed a visual
acuity of only counting fingers bilaterally with mild left side
weakness accompanied by sensory loss to pinprick in the left
arm. There was a left afferent pupillary defect and normal
fundoscopic examination. Her visual ability deteriorated
further to inconsistently identifying light and movement
from the left eye only. She complained of no other symptoms
and denied antecedent trauma or prodromal illness.
She had, however, received her second vaccination against
human papilloma virus 10 days prior to her presentation.
There was no family history of demyelinating disease, collagen-
vascular disease, or rheumatological disorders.
Magnetic resonance imaging (MRI) of the brain
showed swollen enhancement within the chiasm extending
into both retrobulbar optic nerves and a right occipitoparietal
lobe mass (later disclosed as tumefactive
demyelination) with a large zone of surrounding vasogenic
edema (Figure 1). Complete spine MRI was normal.
Biopsy of the hemispheric mass was performed and histology
revealed demyelination (Figures 2 and 3). Subsequent
cultures for aerobic and anaerobic bacteria, fungus, acid
fast bacilli, and examination for parasites were negative
as were serum immunoglobulin G and immunoglobulin
M titers for Toxoplasma gondii. The erythrocyte sedimentation
rate was 16 and the white blood cell count was 6900
with 89% granulocytes and 9% lymphocytes. The patient
received a 5-day course of high-dose intravenous steroids
(1 g methylprednisolone/d divided each 6 hours), followed
by 5 double-volume plasma exchanges with no visual
improvement. Other diagnostic testing included neuromyelitis
optica (neuromyelitis optica-immunoglobulin
G), antinuclear antigen, Sjo¨gren syndrome (SS-A, SS-B),
rheumatoid factor, angiotensin-converting enzyme, which
were all normal or negative. Cerebrospinal fluid analysis
was declined by the patient’s family at this time. The family
refused further therapy with chemotherapy and modulating
agents. Three months after the onset, the patient
still had not regained any visual function, her weakness
and sensory deficit recovered completely however. A
repeat MRI of the brain revealed resolution of the hemispheric
and chiasmal lesions (Figure 4). At 6 months her
funduscopic examination disclosed bilateral optic disc pallor.
A repeat MRI at this time demonstrated no new
lesions and continued resolution of the previously identified
chiasmal enhancement and tumefactive lesion. Again
complete spine MRI was normal. Cerebrospinal fluid was
obtained 6 months after initial symptom onset. Cerebrospinal
fluid cytology was negative for malignancy; additional
studies revealed a clear and colorless fluid with 3 white
eye accompanied by a left side headache. These symptoms blood cells and 0 red blood cells per microliter, glucose
61 mg/dL and simultaneous serum glucose of 91 mg/dL,
protein 30 mg/dL, lactate 1.5 mmol/L, and negative oligoclonal
immunoglobulin G bands. At 18 months after the
onset of her symptoms, her examination remained stable
with no further neurological complaints, persistent profound
visual impairment, inconsistently identifying light
and movement from the left eye only. An MRI of the brain
was performed and was unchanged compared with the
previous one done at 6 months (Figure 5).
Discussion
After a first demyelinating event, the 3 main diagnostic
considerations are multiple sclerosis, acute demyelinating
encephalomyelitis, and neuromyelitis optica. The clinical
symptoms and signs, radiological findings, laboratory
results, and clinical course help determine the likely diagnosis,
with time often being the most crucial component.
On clinical grounds, our patient had bifocal chiasm and
right parieto-occipital lesions occurring 10 days after a
human papilloma virus vaccination, with a rapid progression
over 2 days. There were no further demyelinating events
within the next 18 months. In the context of prior vaccination
in a 16-year-old girl, acute demyelinating encephalomyelitis
is likely to explain the multifocal deficits. This
demyelinating event could also represent the index attack
of neuromyelitis optica known to cause severe bilateral
visual loss due to optic neuritis with poor recovery. Her neuromyelitis
optica-immunoglobulin G antibody was negative.
However, this test has a sensitivity of approximately 70%.
Permanent visual loss is not specific to neuromyelitis optica.
Prior studies of optic neuritis from all etiologies encountered
in childhood have shown good recovery is usual and
that poor visual recovery occurred in less then 20% of children.
9,10 The monophasic course of our patient’s demyelinating
event and the lack of ‘‘dissemination in time,’’ make
a diagnosis of clinically definite multiple sclerosis unlikely.
At this time, a divergence of opinion is notable from authors
of various case series attempting to identify predictive factors
of clinically definite multiple sclerosis in children who
present with a first central nervous system demyelinating
event or initial bilateral optic neuritis.11,12
In this instance, there was no supportive clinical or
laboratory evidence for systemic lupus erythematosus,
Sjo¨gren syndrome, or Lyme infection. Other viral studies
were unrevealing or negative. Bilateral visual loss due to
involvement of the optic chiasm, as revealed on MRI in
our patient, is a rarely described feature of demyelinating
entities. The few reported cases of acute chiasmal neuritis
in the post-MRI era have occurred in the context of infections
with Lyme disease,2 varicella zoster virus,5 postinfectious
Epstein-Barr virus3,4and mumps,6 systemic
lupus erythematosus,7,8 neuromyelitis optica,13,14 and
multiple sclerosis15 (see Table 1). Except in cases caused
by neuromyelitis optica and varicella zoster virus, the clinical
outcomes generally evolved toward improvement of
visual function. It is difficult to assess in retrospect and
therefore not known whether some of the children previously
reported with bilateral optic neuritis also had involvement
of the optic chiasm because it was not specifically
delineated as such in prior reports.
Our patient was also unique in regard to the large tumefactive
plaque identified. Tumefactive lesions can be identified
in both multiple sclerosis and acute demyelinating
encephalomyelitis and thus, are not specific for either. The
international pediatric MS group described tumefactive
lesions as one of the 4 patterns commonly encountered in
acute demyelinating encephalomyelitis.9 These lesions
were also found by Ebner et al16 to heraldmultiple sclerosis
when it starts in childhood. In a recent article, large demyelinating
lesions were significantly more often associated
with monophasic central nervous system demyelinating
events when compared with multiple sclerosis but were not
exclusive to acute demyelinating encephalomyelitis.12 In a
recent review of the literature on tumefactive demyelinating
lesions in childhood carried out by Dastgir and
DiMario,17 50% of these children had subsequent clinical
relapse or developed multiple sclerosis.
Neuromyelitis optica remained a diagnostic consideration
in the patient presented here in spite of the occipito-parietal lesion. An abnormal brain MRI does not
exclude a diagnosis of neuromyelitis optica according to
the recently revised diagnostic criteria.18 Furthermore,
most patients with neuromyelitis optica complicated by
the concurrent development of large brain lesions on MRI
were children.14,19
The radiological resolution of the chiasmal lesion
preceded the occipito-parietal lesion by months. Although
the patient’s left arm weakness improved to complete
recovery promptly on steroid therapy, the visual loss persisted.
This dissociation of the clinico-radiographic evolution
may suggest a clinical feature in favor of acute
demyelinating encephalomyelitis over the progressive
lesions of multiple sclerosis and neuromyelitis optica.
Tumefactive demyelinating lesions are not infrequently
explored surgically because there are no specific
radiologic features that distinguish this acute inflammatory
demyelinating process from a neoplastic one. The histopathology
allows this differentiation in the acute setting
but differentiating between different acquired demyelinating
entities (ie, acute demyelinating encephalomyelitis,
multiple sclerosis, and neuromyelitis optica) has proven
to be a much more complex task. The addition of specific
serum antibody tests and the clinical course over time are
needed at this juncture to secure diagnosis.
Various vaccines have been associated with acute
demyelinating encephalomyelitis, but except for the
Semple vaccine,20 a definite causal effect cannot be
Figure 2. Photomicrograph at low power demonstrating demyelination
on left half of field with a vessel cuffed with lymphocytes. Righthand
side of the field shows white matter with intact myelin (stained
blue) but infiltrated with macrophages. Stained with Holmes Luxol fast
blue, 200 magnification.
Figure 3. Photomicrograph at high power demonstrating a vessel
cuffed with lymphocytes within a field of demyelination and infiltrated
with macrophages. Stained with immunoperoxidase PGM1 for macrophages
(brown), 400 magnification.
established. There have been only 4 cases of central nervous
system demyelination reported in the literature associated
with the fairly new tetravalent vaccine against
human papilloma virus.21 Larger epidemiologic studies
will be needed to confirm a role of the human papilloma
virus immunization and demyelinating disease.
As has been demonstrated in prior reports, the brain
biopsy in this case showed a primary inflammatory demyelinating process without axonal loss. Lymphocytes
and macrophages were present within the plaque and in
the perivenular spaces. These findings do not distinguish
between multiple sclerosis, acute demyelinating encephalomyelitis,
and their variants; a more subtle distinction
may lie in the fact that in multiple sclerosis, inflammatory
cells are generally present throughout the plaque rather
than restricted only to the perivenular cuff, a feature that is more characteristic of acute demyelinating encephalomyelitis.
22
It is possible that human papilloma virus was the
precipitant for the demyelinating event in the patient
presented here. It is tempting to speculate whether there
may be a specific immune mechanism initiated with
human papilloma virus not yet identified, which resulted
in not only acute demyelinating encephalomyelitis but
also in an unusual clinical course that resulted in persistent
visual loss.
References

http://www.theoneclickgroup.co.uk/documents/vaccines/Visual%20Loss%20Following%20Immunization%20Against%20Human%20Papilloma%20Virus.pdf