There are two possible strategies for guaranteeing the numbers. The first is to develop the modern equivalent of a liver pill, an all-purpose cure-all that can be applied to chronic symptoms of every description. Another good strategy is to seize upon a newly defined illness with vague enough symptoms to apply to just about anybody.

Both these strategies may be part of Pfizer’s long-term game plan for Lyrica (pregabalin). The drug was originally approved by the US Food and Drug Administration in 2004 for a highly specific condition: neuropathic (nerve) pain—nerve damage as a result of diabetes or as a complication of shingles (post-herpatic neuropathy, or PHN).

This condition alone represents a sizable market niche; half of the USA’s 18 million diabetics will develop excruciating burning or stabbing pain in the extremities, and 150,000 patients have PHN.

Approval in the UK and elsewhere followed shortly.

Pfizer then decided the new kid on the block might also be able to be used as an adjunctive (chaser) drug to treat partial onset seizures, for which the company received approval in the USA in 2005.

This new indication no doubt stemmed from the great success of their epilepsy drug Neurontin (gabapentin), which Pfizer later discovered could also be used to treat diabetic neuropathy.

Pfizer moved on to a highly lucrative growth market in the form of a mental condition called ‘generalized anxiety disorder (GAD)’, characterized by ‘depressive symptoms and panic, headaches and muscle aches’.

This ‘disorder’, claimed Pfizer, afflicts some two million patients, or 5 per cent of the population at some point in their lives.

If you don’t yet see the connection between Lyrica’s various indications, Pfizer certainly did. Mental symptoms like GAD, claims the company, are far more common with people with chronic medical conditions. People who live with chronic pain or who are wondering if they’re about to have a fit are, not surprisingly, anxious.

Within two years, Pfizer received approval for Lyrica to be used to treat GAD in the European Union.

The drug, an alpha-2-delta ligand, is believed to work by ‘calming hyper-excited neurons’. It appears to bind to a subunit of the calcium channels in the central nervous system and to calm pain receptors and seizures in animal models. When studied in the test tube, it appeared to release several neurotransmitters. Pfizer doesn’t understand its mechanism of action. This, in other words, is a neurochemical looking for a disease.

Although Pfizer conducted studies on more than 9000 patients, adverse events were ‘moderate’. The most common side effects include dizziness (in 29 per cent of patients), sleepiness (22 per cent) and a number of visual disturbances, such as blurred vision (6 per cent), a lack of visual acuity (7 per cent) and visual field changes (13 per cent) (Lyrica manufacturer’s information).

Rats given the drug and studied over their lifetimes developed ocular lesions, including atrophy of the retina and loss of photoreceptor cells and corneal inflammations.

Another side effect of Lyrica is weight gain; about one in 12 patients gain up to 7 percent or more of their body weight. So, if your social anxiety is bound up with a lack of confidence or a poor self-image, this drug could make you feel worse about yourself.
Diabetics gained an average of 5.2 kg (11.5 pounds) and as much as 16 kg (35 pounds). This is a particular concern for diabetics, since weight gain can often send blood sugar levels spiralling out of control.

Aside from piling on the pounds, some 6 per cent of patients suffer water retention in the extremities. In diabetics, problems of weight gain and water retention escalated (7.5 per cent and 19 per cent, respectively) among patients taking both Lyrica and a thiazolidinedione anti-diabetic drug.

Diabetics should also note that animals given this drug developed skin ulcerations, from erythema or necrosis (skin death), although these effects weren’t observed in human trials.

More worrying, the drug has demonstrated a high incidence of haemangiosarcoma (cancer in the blood vessels) among two strains of mice. What this means, as animal studies don’t always apply to humans, is anyone’s guess.

Besides possibly causing cancer, the drug causes a decrease in blood platelet counts, with 5 per cent of patients suffering a significant decrease. Lowered levels of blood platelets affect the ability of the blood to clot and may precipitate haemorrhage.

Patients who take pregabalin also demonstrate worrying changes in electrocardiogram readings, called a prolongation of the PR interval. This condition is seen in alcoholics after binge drinking (Neth J Med, 2005; 63(2): 59–63) and predisposes to interrupted electrical impulses to heart muscles, arrhythmia and possibly cardiac arrest.

The drug also causes elevations in levels of creatine kinase, an enzyme in the muscles. When muscles are injured this enzyme leaks out into the blood stream. Elevated levels (also commonly caused by statins) are often associated with myopathy, or muscle weakness.

Finally, you might think twice about this drug if you want to have a baby, particularly if you are the male partner. In various animal models, the drug lowered sperm count, increased sperm abnormalities, reduced fertility and caused miscarriages and birth defects. Nevertheless, in the one short-term study carried out in men the drug lowered sperm count, but not to a pronounced degree.

It’s probably not such a good idea to give it to children, either. Young animals given the drug suffered difficulties with motor skills and learning, even after the drug was withdrawn.

Lynne McTaggart

Trigeminal neuralgia usually presents with severe unilateral facial pain. Its cause is unclear but the painful facial spasms are often precipitated by cold or wind. The Chinese claim to be able to gain some improvement, with acupuncture, in about 70 per cent of cases of trigeminal neuralgia. Judging by the experience of Western acupuncturists this success rate represents a rather high figure, although acupuncture can undoubtedly have a beneficial effect on this type of pain.

Postherpetic neuralgia is the pain that occurs after an attack of shingles. Shingles is a viral infection of the nerves, and the nerves affected by shingles can occasionally continue to cause severe pain after the shingles has cleared.

Postherpetic neuralgia is an uncommon disease in China; this may be because the Chinese treat all cases of shingles with acupuncture before the postherpetic neuralgia can develop. There are other possible explanations for its decreased incidence in China, perhaps postherpetic neuralgia is affected by diet, or racial characteristics; however, it is much more reasonable to suggest that the dearth of postherpetic neuralgia in China is due to the daily treatment of shingles with acupuncture. It seems that of those patients with established postherpetic neuralgia, about 40 per cent gain some degree of long term benefit from acupuncture. If this figure could be substantiated with proper clinical research work, it would represent a significant advance in the treatment of this condition.

There are a vast number of aches and pains that are often described as neuralgic. Many of these occur as facial pain and most of them cause severe discomfort. It is always worth while to attempt to alleviate these pains by using acupuncture. Some people respond and others do not; it is impossible to give figures for success, or even estimates, without going into great detail about the exact cause and type of neuralgia being treated.

Alzheimer’s disease is the most common form of dementia in the
United States. It and related
dementias affect at least 2 million, and possibly as many as 4
million, U.S. residents. Despite its
prevalence, dementia often goes unrecognized or is misdiagnosed
in its early stages. Many
health care professionals, as well as patients and family
members, mistakenly view the early
symptoms of dementia as inevitable consequences of aging.

Some disorders that result in dementia are “reversible or
potentially reversible,” which means
that they can be treated effectively to restore normal or nearly
normal intellectual function.
Among the most frequent reversible causes of dementia are
depression, alcohol abuse, and drug
toxicity. In elderly persons, drug use—particularly drug
interactions caused by
“polypharmacy” (simultaneous use of multiple drugs)—is a
common cause of cognitive
decline. Depression also is an underdiagnosed condition in this
population.

The majority of dementias, including Alzheimer’s disease, are
considered nonreversible. Even
for these conditions, correct diagnosis of the problem in its
early stages can be beneficial.
Correct recognition can prevent costly and inappropriate
treatment resulting from misdiagnosis,
and give patients and families time to prepare for the
challenging financial, legal, and medical
decisions that may lie ahead. In addition, many of the
nonreversible dementias such as
Alzheimer’s disease include symptoms that can be treated
effectively (for example, incontinence,
wandering, depression).

According to the National Institute on Aging, an estimated $90
billion is spent annually for
Alzheimer’s disease alone, and the noneconomic toll is
incalculable. Although State and local
governments and the Federal Government bear some of the economic
burden, largely through
Medicare and Medicaid, a substantial proportion is borne by
families that provide unpaid care.
Changes caused by dementia may advance relentlessly over many
years, creating not only deep
emotional and psychological distress but practical problems
related to caregiving that can
overwhelm affected families.

Addressing the Problem

In 1992, the Agency for Health Care Policy and Research, a
Federal Government agency within
the Public Health Service, convened a panel of private-sector
experts to develop a clinical
practice guideline on screening for Alzheimer’s disease and
related dementias. This topic was
selected because:

• Dementia in the adult population is a serious and growing
  medical, social, and economic
  problem.

• Alzheimer’s disease and related dementias exact a massive
  toll in health care costs,
  disability, and lost productivity of both patients and family
  caregivers.

• Early symptoms of dementia are commonly overlooked,
  mistakenly attributed to normal
  aging, or misdiagnosed.

• Failure to diagnose early-stage dementia can result in
  needless and possibly harmful
  treatment.

After extensive literature searches and meta-analyses, the panel
decided to focus on early
detection of dementia in persons exhibiting certain
characteristics or triggers that signal the need
for further assessment, rather than recommend general screening
of segments of the population,
such as those over a certain age. The panel made this decision
after concluding that:

• No evidence exists to support recommending some of the most
  frequently used screening
  tests over others.

• None of the tests has a high sensitivity for early or mild
  dementia.

• No evidence supports the efficacy of a general screen for
  Alzheimer’s disease or related
  dementias, given the lack of unequivocally effective treatment
  and the difficulty of
  recognizing early dementia.

The panel subsequently limited its scope specifically to the
subject of recognition and initial
assessment and therefore did not address differential diagnosis,
management, or treatment issues
after diagnosis.

Principal Objective

The panel’s principal objective was to increase the likelihood of
early recognition and assessment
of a potential dementing illness so that (1) concern can be
eliminated if it is not warranted; (2)
treatable conditions can be identified and addressed
appropriately; and (3) nonreversible
conditions can be diagnosed early enough to permit the patient
and family to plan for
contingencies such as long-term care.

Specifically, the panel’s goals were to:

• Improve the detection of Alzheimer’s disease and related
  dementias in their early stages
  in persons exhibiting certain signs and behaviors.

• Educate health professionals, patients, and their families
  about symptoms that suggest the
  need for an initial assessment for a dementing disorder.

• Identify areas for further research on early recognition of
  dementia.

Findings

The panel’s major findings include:

• Certain triggers should prompt a clinician to undertake an
  initial assessment for dementia
  rather than attribute apparent signs of decline to aging.

• An initial clinical assessment should combine information
  from a focused history and
  physical examination, an evaluation of mental and functional
  status, and reliable
  informant reports. It also should include assessment for delirium
  and depression.

• An assessment instrument known as the Functional Activities
  Questionnaire is a
  particularly useful informant-based measure in the initial
  assessment for functional
  impairment.

• Among effective mental status tests, the Mini-Mental State
  Examination, the Blessed
  Information-Memory-Concentration Test, the Blessed
  Orientation-Memory-Concentration Test, and the Short Test of
  Mental Status are largely
  equivalent in discriminative ability for early-stage
  dementia.

• Clinicians should assess and consider factors such as
  sensory impairment and physical
  disability in selection of mental and functional status tests,
  and other confounding factors
  such as age, educational level, and cultural influences in
  interpretation of test results.

In asymptomatic persons who have possible risk factors (e.g.,
family history and Down
syndrome for Alzheimer’s disease), the clinician’s judgment and
knowledge of the patient’s
current condition, history, and social situation (living
arrangements, support services, isolation)
should guide the decision to initiate an assessment for
dementia.

Initiating an Assessment

For a diagnosis of dementia, current criteria in the Diagnostic
and Statistical Manual of Mental
Disorders, Fourth Edition (DSM-IV), require evidence of decline
from previous levels of
functioning and impairment in multiple cognitive domains, not
solely memory. Because
evidence of decline in previous abilities is critical in
establishing dementia, a personal
knowledge of the patient is invaluable to the clinician in
assessing symptoms and interpreting
results of an initial assessment for dementia.

A focused history is critical in the assessment for dementia. It
is particularly important to
establish the symptoms’ mode of onset (abrupt versus gradual);
progression (stepwise versus
continuous decline; worsening versus fluctuating versus
improving), and duration.

A focused physical examination, including a brief neurological
evaluation, is an essential
component of the initial assessment. Special attention should be
placed on assessing for those
conditions that cause delirium, since delirium represents a
medical emergency. During the
focused physical examination, health care providers should be
alert to signs of abuse and neglect
of patients by caregivers and report suspected abuse to the
proper authorities.

Informant reports (information obtained from family members or
caregivers) can supplement
information from patients who have experienced memory loss and
may lack insight into the
severity of their decline. Health care providers, however, should
consider the possibility of
questionable motives of informant reports, which may exaggerate,
minimize, or deny symptoms.

Brief mental status tests can be used but they are not
diagnostic. They are used to (1) develop a
multidimensional clinical picture; (2) provide a baseline for
monitoring the course of cognitive
impairment over time; (3) reassess mental status in persons who
have treatable delirium or
depression on initial evaluation; and (4) document multiple
cognitive impairments as required
for a diagnosis of dementia.

Assessing for Depression

Depression can be difficult to distinguish from dementia, and it
can coexist with dementia.
Changes in memory, attention, and the ability to make and carry
out plans suggest depression,
the most common psychiatric illness in older persons. Marked
visuospatial or language
impairment suggests a dementing process. The clinical interview
is the mainstay for evaluating
and diagnosing depression in older adults. Two self-report
instruments with established
reliability and validity are the Geriatric Depression Scale (GDS)
and the Center for
Epidemiological Studies Depression Scale (CES-D).

Interpreting Findings

Three results are possible from the combination of findings from
assessments of mental and
functional status: (1) normal, (2) abnormal, and (3) mixed.

When results of both mental and functional status tests are
normal and there are no other clinical
concerns, reassurance and suggested reassessment in 6 to 12
months are appropriate. If concerns
persist, referral for a second opinion or further clinical
evaluation should be considered.

When both mental and functional status tests yield findings of
abnormality, further clinical
evaluation should be conducted. However, a laboratory test should
not be used as a screening
procedure or part of an initial assessment. Laboratory tests
should be conducted only after (1) it
has been confirmed that the patient has impairment in multiple
domains that is not lifelong and
represents a decline from previous levels of functioning; (2)
delirium and depression have been
excluded; (3) confounding factors such as educational level have
been considered; and (4)
medical conditions have been be ruled out.

Mixed results—abnormal findings on the mental status test
with no abnormalities in
functional assessment or vice versa—call for further
evaluation. For example:

• Patients who have abnormal results on only the mental
  status test require more complete
  testing. Results that indicate possible neuropsychiatric or
  systemic neurological problems
  call for referral to an appropriate specialist.

• Patients who have declining function but normal mental
  status test results require either
  (1) further neurological evaluation for systemic neurological
  diseases or (2) psychiatric
  or psychological evaluation if evidence suggests depression or
  other emotional problems.

The Role of Neuropsychological Testing

Neuropsychological tests can examine performance across different
domains of cognition. This
broad battery of tests can help in identifying dementia among
persons with high premorbid
intellectual functioning, discriminating patients with a
dementing illness from those with focal
cerebral disease, and differentiating among certain causes of
dementia.

The Importance of Followup

Followup, with assessment of declining mental function, may be
the most useful diagnostic
procedure for differentiating Alzheimer’s disease from normal
aging. For this reason, the mental
status test should be repeated over a period of 6 to 12 months.
In cases of referral, it is important
to make sure that test results and medical records follow the
patient from the specialist back to
the referring clinician.

Key Points About Alzheimer’s Disease

Key Points About Alzheimer’s Disease

• Although changes in memory or cognition may accompany
  normal aging, significant
  impairment and disability are not a part of normal aging.

• It is important for clinicians, as well as patients and
  family members, to recognize
  symptoms that should trigger an initial assessment for
  dementia.

• Some causes of dementia can be treated effectively to
  eliminate or greatly improve
  cognitive performance.

• Among older persons, depression and interactions from
  multiple medications are two
  common and highly treatable causes of dementia symptoms.

• An initial assessment for dementia can (1) lead to
  effective treatment of causes; (2)
  prevent unnecessary and possibly harmful treatment resulting from
  misdiagnosis; and (3)
  avoid the trauma of a diagnosis of dementia or Alzheimer’s
  disease where it does not
  exist.

• The prolonged course of deterioration found in many
  dementias takes a major emotional,
  psychiatric, and physical toll among family members and
  caregivers.

• Learn more about symptoms that may indicate early-stage
  dementia and how to conduct
  an initial assessment. Read Recognition and Initial Assessment
  of Alzheimer’s Disease
  and Related Dementias, Clinical Practice Guideline
  No. 19, and use its companion Quick
  Reference Guide for Clinicians. Give the Consumer
  Version to patients, family members,
  and other caregivers.

For Patients

• Dementia is different from normal aging. Only certain tests
  can show that difference.
  Symptoms that suggest Alzheimer’s disease or a related dementia
  should be brought to
  the attention of the family’s health care provider as soon as
  possible.

• Some memory and other problems can improve or disappear
  with appropriate treatment.

• Although there is not yet a clearly effective treatment for
  Alzheimer’s disease, resources
  are available to help patients and families cope with this
  condition and prepare for the
  future.

• Order the consumer booklet, Early Alzheimer’s
  Disease: from the U.S. Government’s
  Agency for Health Care Policy and Research. It provides
  information about the early
  stages of Alzheimer’s disease and similar illnesses. It also
  includes a list of resources
  where readers can find out more about the medical, financial, and
  social support services
  that are available in their communities.

• The Agency for Health Care Policy and Research also has a
  Clinical Practice Guideline
  and a Quick Reference Guide for health care providers
  about early identification of
  Alzheimer’s disease and other forms of dementia.

Symptoms That Might Indicate Dementia

Does the person have increased difficulty with any of the
activities listed below? Positive
findings in any of these areas generally indicate the need for
further assessment for the presence
of dementia.

• Learning and retaining new information. For example:
  is more repetitive; has more
  trouble remembering recent conversations, events, appointments;
  more frequently
  misplaces objects.

• Handling complex tasks. For example: has more
  trouble following a complex train of
  thought, performing tasks that require many steps such as
  balancing a checkbook or
  cooking a meal.

• Reasoning ability. For example: is unable to respond
  with a reasonable plan to problems
  at work or home, such as knowing what to do if the bathroom
  flooded; shows
  uncharacteristic disregard for rules of social conduct.

• Spatial ability and orientation. For example: has
  trouble driving, organizing objects
  around the house, finding his or her way around familiar
  places.

• Language. For example: has increasing difficulty
  with finding the words to express what
  he or she wants to say and with following conversations.

• Behavior. For example: appears more passive and less
  responsive; is more irritable than
  usual; is more suspicious than usual; misinterprets visual or
  auditory stimuli. In addition
  to failure to arrive at the right time for appointments; the
  clinician can look for difficulty
  discussing current events in an area on interest and changes in
  behavior and dress. It
  might also be helpful to follow up on areas of concern by asking
  the patient or family
  members relevant questions.

Guideline Development

The Agency for Health Care Policy and Research convened an
18-member private-sector,
interdisciplinary panel composed of psychologists, psychiatrists,
neurologists, an internist,
geriatricians, nurses, a social worker, and consumer
representatives. The panel conducted
extensive literature searches to identify empirical studies of
assessment of mental status
instruments for differentiating persons with and without dementia
and instruments used in the
assessment of persons with Alzheimer’s disease. It conducted
additional literature searches
related to assessment of functional impairment and risk factors
for dementia and conducted
meta-analyses. The panel also held a public hearing to give
interested organizations, individuals,
and agencies an opportunity to present oral or written testimony
for the panel’s consideration.

The results of the literature reviews and meta-analyses were used
to develop a draft guideline.
Copies were distributed for two peer review cycles. Reviewers
were selected to represent a broad
range of disciplines and clinical practice areas. A total of 109
reviewers submitted comments,
which were collated and reviewed by the panel co-chairs and used
to develop the final guideline.

Current Availability

You can now obtain copies of the Consumer Version free
through InstantFAX, which operates
all day every day. Using a fax machine equipped with a touch tone
telephone, dial (301)
594-2800, push 0 and follow the voice prompts. The code for the
publication is 967123.

Future Availability

Additional guideline information will be available later this
year (Winter 1996) in several forms:

• Clinical Practice Guideline, intended for the health
  care provider, contains a discussion
  of the issues and the panel’s findings and recommendations, with
  supporting evidence
  and references. It also includes a series of tables and a flow
  chart summarizing the panel’s
  recommended approach to early recognition and initial assessment
  of suspected
  dementia.

• Quick Reference Guide for Clinicians, also intended
  for health care providers, is a brief
  summary of and companion piece to the Clinical Practice
  Guideline. It provides
  highlights of initial assessment and interpretation of findings
  and presents the tables and
  flow chart.

• Consumer Version, published in English and Spanish,
  is a brochure for patients, their
  families, and the general public that describes the problem,
  outlines procedures for
  identifying dementia in its early stages, and provides resource
  information for those who
  must deal with a diagnosis of probable Alzheimer’s disease or a
  related dementia.

To obtain further information on the availability of the Quick
Reference Guide or Consumer
Version, call the AHCPR Publications Clearinghouse at (800)
358-9295 or write to:

Alzheimer’s Disease
AHCPR Publications Clearinghouse
P.O. Box 8547
Silver Spring, MD 20907-8547

Single and bulk copies of the Clinical Practice Guideline,
Recognition and Initial Assessment of
Alzheimer’s Disease and Related Dementias, may be purchased,
when available, from the U.S.
Government Printing Office by calling (202) 512-1800.

The Clinical Practice Guideline, Quick Reference Guide, and
Consumer Version will also be
available on the Internet through the AHCPR Home Page. You can
access the guideline products
by using a Web browser, specifying the URL http://www.ahcpr.gov/guide, and clicking on
Clinical Practice Guidelines Online.

AHCPR, a part of the U.S. Public Health Service, is the lead
agency charged with supporting
research designed to improve the quality of health care, reduce
its costs, and broaden access to
essential services.

U.S. Department of Health and Human Services
Public Health Service
Agency for Health Care Policy and Research
2101 East Jefferson Street, Suite 501
Rockville, MD 20852

AHCPR Publication No. 97-R123
September 1996

Sutherland reasoned that these joints could only make sense if they contributed towards motion between the bones. Against all the accepted medical thinking he reasoned, studied and observed the cranial structures and their functions, with a view to establishing what these were. Gradually, over many years he came to understand the inter-relationship between the bony structures of the cranium and its contents and functions. These include not only the nerve and brain tissues but strong fibrous bands which divide and support the various areas of the brain and which are intimately involved in the motion of the cranial structures. The two main tension membranes are the Falx Cerebri and the Tentorium Cerebeli.

Infant Cranium Showing: 1. Anterior Fontanelle; 2. Posterior Fontanelle.

The erroneous belief that the skull is a rigid bony structure, and that the sutures are immovable arose from anatomists studying these structures from dried specimens. The study of living bones is quite different. It is a simple matter to feel the resilience of the skull in the living skull, even into adult life.

The bones that make up the skull are, in health, movable and do in fact, move in a rhythmic manner throughout life. The range of this movement is small, but to the trained hand, easily felt. Since nothing in the body is without purpose, this function is reasoned as contributing to the normal running of the body. It might be argued that what is felt is no more than a resiliency, a plasticity, which would be necessary. to avoid the skull being over rigid, and thus in danger of fracturing in case of a blow. This is partly true, but does not explain the rhythmic expansion and contraction that takes place in the skull, independent of the normal respiration and heart beat.

Primary Respiratory Mechanism

Research over the past half century has demonstrated that this movement is part of a mechanism which has been named the ‘primary respiratory mechanism’. This involves not only the skull bones, and their contents but, by virtue of strong fibrous tissue connections, the spinal column and the sacrum (the triangular bony structure at the base of the spine). As these structures move (much as the diaphragm and chest move in breathing, but on a much smaller scale) an important circulatory function is being carried out in the skull and throughout the body. Blood and cerebro-spinal fluid are pumped through the intricate channels surrounding the structures of the brain and the central nervous system.

It has been shown under the electron-microscope that the tissue which binds all other tissues together, the connective tissue, or fascia, of the body, has a tubular structure. The cerebro-spinal fluid permeates these structures and carries with it hormonal secretions vital to the health of the body. The most important glands in the body lie within the skull, and their ability to function is now known to be influenced by the efficiency, or otherwise, of the primary respiratory mechanism.

What does all this mean in terms of health and disease? It explains a good deal that was previously unexplained, and opens up the possibility of treating conditions that have proved untreatable or stubbornly resistant to treatment, by more conventional methods.

Illustrates cranial manipulation aimed at restoring normal mobility between the zygomatic and the temporal bones. This treatment is extremely gentle. No force is used, only a holding of the appropriate bones whilst the patient’s respiratory effort creates the corrective

If in adult life there occur blows to the head, whiplash injuries to the neck, heavy dental extractions, blows to the base of the spine, even more subtle structural pressures resulting from new dentures, then the complex mechanism, described above, can be interfered with and a variety of symptoms, local and distant can occur. Local conditions that commonly result from this type of cause include tinnitus (ringing in the ears), Meniere’s disease (loss of balance), facial neuralgia, migraine and other headaches, visual disturbances, jaw dysfunction (difficulty in chewing or in opening the mouth) etc. Distant effects can include any sudden changes in the metabolism of the body which could have hormonal origins.

Treatment of Cranial Distortion in New-born Babies

A vast range of conditions have been helped by cranial osteopathy’s ability to positively influence the hormonal balance. Such conditions as rheumatoid arthritis, multiple sclerosis, fluid retention, asthma and other allergic problems have all been favourably (together with other natural methods) influenced. The most exciting and important application of this approach is, however, in the treatment of babies and children who have suffered cranial distortion before, during, or soon after birth.

A variety of factors can affect the soft bones and cartilaginous structures of the foetus before, and during birth, and of the infant, soon after. If the mother-to-be has a spinal curve or an acute lumbar curve (hollow back) then the developing foetus may lie in such a way as to crowd or warp, the skull bones. If labour is induced, and the mother’s birth canal has not had the opportunity to soften and prepare for the engagement of the foetal head, or if the birth is too rapid and the contractive forces acting on the foetal head are too powerful, or if the process of labour is too long and difficult, the effect on the soft head bones and their supporting structures (tension membranes etc. ) can be to so mould them that a return to normal never takes place. If instrument delivery is clumsy this too can cause cranial distortion, and long term problems. This is not to say that forceps delivery is always harmful, indeed it often prevents even worse damage, but it certainly can cause damage, wrongly applied.

If a baby is born prematurely, and is laid on a normal surface then the very weight of the head can have a compressing and warping effect. After all, the foetus has been cushioned in fluid, and a water bed would be a better start as a surface on which to lie, for such a newcomer.

If a newborn child cries too much, refuses food, is stiff and difficult to handle, has sleeping problems, has swallowing difficulty or even shows a distinct preference to lie on one side or not to lie on its back, or is dopey and just ‘too good’, taking no interest in anything, or rubs or bangs its head, or fails to develop normally, then chances are that there is a cranial distortion. All such children should be seen as soon as possible by a cranial osteopath, as should all cases of cerebral palsy and spasticity.

The treatment methods are exceedingly gentle, and treatment can be started within hours of birth. There is no heroic pushing and pulling which so many people associate with conventional osteopathy, but a gentle, subtle attempt to restore structural normality and with it functional normality (health). Learning the specialized techniques of cranial osteopathy requires lengthy and diligent study and practice. The anatomy and physiology of the skull, and its relationship with other spinal and body structures and functions, is a demanding study. Sensitive and subtle manual skills are required in the application of cranial manipulation, which is not so much concerned with altering the position of bones as with releasing articular strains between the structures and restoring physiological motion. As has been stated, it is in infants and the new-born that the greatest good can be achieved. The following quotation from The Selected Writings of Beryl Arbuckle D. O. published in the USA by The National Osteopathic Institute and Cerebral Palsy Foundation (1977) illustrates this:

The under-developed cerebro-spinal system of the newborn is housed by an immature cranium and vertebral canal. To the skull, with all its intricate construction, so often taken for granted, its physiological movement, little considered and less understood, is attributed the function of protecting the brain. The infant skull is very immature having little ossification and many of the bones are in separate parts, cartilaginous and membranous. The vault consists of very thin bones with but one layer and no bony sutures. The overriding thus possible during delivery is one of nature’s provisions for the reduction of cranial size to better enable the passage of the head through the birth canal. If, by chance, for any one of a hundred reasons, that infant is unable to reduce to the full extent this natural moulding it is impossible to prognosticate the severity of the symptoms which may be manifested in later life on account of the persistent unnatural strain throughout the stress bands of the aural membranes. ‘An osteopath sees cause in a slight anatomical deviation for the beginning of disease’ (A. T. Still). There may result severe or slight muscular handicaps, mental difficulties, from idiocy to mere confusion or general slowness, inability or instability.
The physician who is able to recognize these deviations and able to make the necessary corrections intelligently at the very first sign of slight difficulty, often years before serious symptoms could be manifested, while the child is still in the developing or growing stage, will turn the trouble of today into the triumph of tomorrow.

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For stress in general, try bergamot, chamomile, lavender, melissa, clary sage, neroli, rose or jasmine. For insomnia due to mental agitation or overwork, clary sage, marjoram, ylang-ylang and neroli can help you unwind. Headaches due to nervous tension are also helped by these oils, but keep in mind that headaches can result from many causes, from indigestion to hormonal problems, and should be treated appropriately.

Relaxing/Antidepressant Formula

3 drops lavender

3 drops neroli

2 drops marjoram

2 drops ylang-ylang

1 drop chamomile

2 drop clary sage

1 ounce carrier oil

This can be used as a massage or bath oil.

Neuralgia, or nerve pain, is best remedied by treating the cause, although essential oils do alleviate the pain, especially when used in conjunction with massage.

Neuralgia Relief

5 drops helichrysum

3 drops chamomile

2 drops marjoram

2 drops lavender

1 ounce carrier oil

Combine ingredients and use for massage.

Herbal Adjuncts-Herbs can stimulate or relax the nervous system. A number of plants are relaxing, including California poppy (completely safe, with no addictive alkaloids), hops, valerian, passionflower and catnip.

One of the best tonics to repair the nervous system is wild oats (even eating oatmeal does some good); others include skullcap and vervain. St. John’s wort repairs damaged nerves and helps overcome depression.

Like most other B vitamins, thiamine is needed in regular supply, though after its absorption from the upper and lower small intestine, some B1 is stored in the liver, heart, and kidneys. Most excess thiamine is eliminated in the urine; some seems to be excreted in the sweat as well.

Sources: Since thiamine is lost in cooking and is depleted by use of sugar, coffee, tannin from black teas, nicotine, and alcohol, it is necessary to insure that intake of thiamine is optimal. There are a number of food sources for thiamine; however, they may not be the everyday fare for many people. Good sources of vitamin B1 include the germ and bran of wheat, rice husks (outer covering), and the outer portion of other grains. With the milling of grains and use of refined flours and white or “polished” rice, many of us are no longer getting the nourishment of thiamine that is available when we eat wholesome, unprocessed foods.

Other good sources of thiamine besides wheat germ and bran, whole wheat or enriched wheat flour, and brown rice are brewer’s yeast and blackstrap molasses. Oats and millet have modest amounts, as do many vegetables, such as spinach and cauliflower, most nuts, sunflower seeds, and legumes, such as peanuts, peas, and beans. Of the fruits, avocado is the highest in vitamin B1. Pork has a high amount of this B vitamin. Many dried fruits contain some thiamine, though the sulfur dioxide often added as a preservative seems to destroy this vitamin.

Functions: Thiamine helps a great many bodily functions, acting as the coenzyme thiamine
pyrophosphate (TPP). It has a key metabolic role in the cellular production of energy, mainly in glucose metabolism. Thiamine is also needed to metabolize ethanol, converting it to carbon dioxide and water. B1 helps in the initial steps of fatty acid and sterol production. In this way, thiamine also helps convert carbohydrate to fat for storage of potential energy.

Thiamine is important to the health of the nerves and nervous system, possibly because of its role in the synthesis of acetylcholine (via the production of acetyl CoA), an important neurotransmitter. With a lack of vitamin B1, the nerves are more sensitive to inflammation. Thiamine is linked to individual learning capacity and to growth in children. It is also important to the muscle tone of the stomach, intestines, and heart because of the function of acetylcholine at nerve synaptic junction. It is conceivable that adequate thiamine levels may help prevent the accumulation of fatty deposits in the arteries and thereby reduce the progression of atherosclerosis.

Uses: Vitamin B1 is, of course, used to treat any of the symptoms of its deficiency or its
deficiency disease beriberi (discussed below). It is used in the treatment of fatigue, irritability, low morale, and depression and to prevent air- or seasickness. It seems to help the nerves, heart, and muscular system function well. By aiding hydrochloric acid
production, thiamine may help digestion or reduce nausea, and it can remedy constipation by increasing intestinal muscle tone. Thiamine is used commonly to improve healing after dental (or, often, any) surgery.

Increased thiamine intake may be suggested for numerous mental illnesses and problems that affect the nerves. These include alcoholism and its nerve problems, multiple sclerosis, Bell’s palsy (a facial nerve paralysis), and neuritis. Treatment with thiamine, for example, has been helpful in decreasing the sensory neuropathy that accompanies diabetes and in lessening the pain of trigeminal neuralgia. Thiamine also has a mild diuretic effect and is supportive of heart function, so it is suggested in the treatment program for many cardiovascular problems.

Since thiamine is eliminated through the skin somewhat, doses of over 50-100 mg. per day may help repel insects such as flies and mosquitos from those with “sweet blood.” Other uses for increased thiamine include treatment of stress and muscle tensions, diarrhea, fever and infections, cramps, and headaches.

Deficiency and toxicity: There is no known toxicity in humans from thiamine taken orally.
People have taken hundreds of milligrams daily without any harmful effect, although some may become more stimulated than others. Thiamine injections, however, have occasionally been associated with trauma or edema.

Prolonged restriction of thiamine intake may produce a wide variety of symptoms, particularly affecting the general disposition, nervous system, gastrointestinal tract, and heart. With thiamine deficiency, as with deficiency of most any essential nutrient,
symptoms range from mild to moderate depletion disorders to the serious disease state that RDA amounts usually prevent.

Beriberi is the name given to the disease caused by thiamine deficiency. There are three basic expressions of beriberi, namely childhood, wet, and dry beriberi. Childhood beriberi stunts the growth process, and in infants high-pitched scream and rapid heartbeat are associated with the disease. Wet beriberi is the classic form with edema (swelling) in the feet and legs, spreading to the body, and associated decreased function of the heart. Dry beriberi is not accompanied by swelling but seems to be manifested by weight loss, muscle wasting, and nerve degeneration. Another thiamine deficiency disease involves degeneration of the brain and affects the general orientation, attitude, and ability to walk. This has been termed the Wernicke-Korsakoff syndrome and is usually seen in people who have been addicted to alcohol for many years.

These severe problems can and do lead to death when they are not corrected with dietary change or supplemental thiamine. Before vitamin B1 was discovered, this affected many people who ate a diet consisting mainly of polished rice. Today, deficiency of this vitamin is still quite common. Although it does not usually lead to beriberi, a number of symptoms can result from a depletion of thiamine body levels. A low-B1 diet consisting of polished rice or unenriched white flour is not often the culprit in our culture. The diet that contributes to deficiency today, especially among teenagers, is high in colas, sweets, fast foods, and many other empty-calorie foods. This diet can also lead to skin problems and symptoms of neurosis, almost like a Jekyll-and-Hyde disposition.

With a deficiency of thiamine, carbohydrate digestion and the metabolism of glucose are diminished. There is a build-up of pyruvic acid in the blood, which can lead to decreased oxygen utilization and therefore mental deficiency and even difficulty in breathing. While B1 is needed for alcohol metabolism, alcohol abuse is often associated with a poor diet and poor B1 absorption. The poor perceptions, mental states, and nerve problems that come with alcoholism may be associated with thiamine deficiency.

The first symptoms of thiamine deficiency may be fatigue, instability. These may be followed by confusion, loss of memory, depression, clumsiness, insomnia, gastrointestinal disturbances, abdominal pain, constipation, slow heart rate, and burning
chest pains. As the condition progresses, there may be problems of irregular heart rhythm, prickling sensation in the legs, loss of vibratory sensation, and the muscles may become tender and atrophy. The optic nerve may become inflamed and the vision will be affected.

Generally, with low B1 the central nervous system–the brain and nerves–does not function optimally. The gastrointestinal and cardiovascular systems are also influenced greatly. Vitamin B1 levels have been shown to be low in many elderly people, especially those that experience senility, neuroses, and schizophrenia. We might question how much of the degeneration and disease of old age may be a result of withering digestion and assimilation, leading to deficiencies of various vitamins and other necessary nutrients.

Requirements: The RDA for vitamin B1 is about 1.2 mg. per day, or 1.4 mg. during
pregnancy or lactation. Infants need more per body weight though less in total, about 0.5 mg. per day. Thiamine needs are based on many factors; given good health, we need about 0.5 mg. per 1,000 calories consumed, since B1 is required for energy metabolism. So our needs are based on body weight, calorie consumption, and the amount of vitamin B1 synthesized by intestinal bacteria, which can vary greatly from person to person.

Thiamine needs are also increased with higher stress levels, with fever or diarrhea, and during and after surgery. Those who smoke, drink alcohol, consume caffeine or tannin from coffee or tea, or who are pregnant, lactating, or taking birth control pills all need more thiamine, possibly much more than the RDA, for optimum health.

Thiamine is needed in the diet or in supplements daily. There are some stores in the heart, liver, and kidneys; however, these do not last very long. The minimum B1 intake for those who are very healthy is at least 2 mg. per day. A good insurance level of thiamine is probably 10 mg. a day, though even higher levels may be useful in some situations. When we do not eat optimally, have any abusive substance habits (especially alcohol abuse), or are under stress, increased levels of thiamine are recommended. An example is the B complex 50 products–that is, 50 mg. of B1 along with that amount of most of the other B
vitamins–suggested as a daily regimen. The upper intake levels of thiamine should not be much more than 200-300 mg. daily. Often B1, B2 (riboflavin), and B6 (pyridoxine) are formulated together in equal amounts within a B-complex supplement. When people take higher amounts of the B vitamins, many feel a difference in energy and vitality. (Note: Riboflavin taken for any length of time is best limited to 50 mg. daily.)

Vitamin B12 (Cobalamin) is named the “red vitamin,” as it is a red crystalline compound.
B12 is unique in that it is the only vitamin that contains an essential mineral–namely, cobalt. Cobalt is thereby needed to make B12 and so is essential for health. B12 is unique also in that it is required in much tinier amounts than the other B vitamins. Only 3-4 mcg. (micrograms, or thousandths of a milligram) are needed at minimum; however, higher levels, up to 1 mg., are often used therapeutically.

Vitamin B12 is a very complex molecule. Besides cobalt, it also contains carbon, oxygen, phosphorus, and nitrogen. Cobalamin is stable to heat, though sensitive in heated acid or alkali solution, slightly sensitive to light, and destroyed by oxidizing and reducing agents and by some heavy metals.

Vitamin B12 was isolated in 1926 as the factor that treated a feared disease, pernicious anemia–termed “pernicious” because it could be fatal, most often from neurologic degeneration. But the substance cobalamin, when given orally (actually liver was used as the cure; it contains high amounts of B12), did not cure all of the people with the disease, and some people still developed pernicious anemia. It was later found that a mucoprotein enzyme produced by the stomach (by the parietal cells that also make hydrochloric acid) was also needed for vitamin B12 to be absorbed into the body from the intestines. This enzyme has been termed the “intrinsic factor,” while vitamin B12 is the “extrinsic factor.” Aging, stress, and problems with the stomach or stomach surgery weaken the body’s ability to produce the “intrinsic factor”; also, some people appear to have a genetic predisposition that makes them more prone to pernicious anemia. Hydrochloric acid helps the absorption of B12; if acid production is weak, the absorption is lessened. Calcium and thyroid hormone assist as well. Pregnancy, absorb this important vitamin. Aging more
likely lessens some of the many factors needed for ideal absorption of B12, so deficiency symptoms are more common in older people.

Cobalamin is absorbed primarily from the last part of the small intestine, the ileum. In the blood, it is bound to a protein globulin to be carried to the various tissues. The body actually stores vitamin B12, so any deficiencies may take several years to develop. The
highest concentrations of B12 are found in the liver, heart, kidney, pancreas, brain, testes, blood, and bone marrow–all active metabolic tissues. The “red vitamin” is very important to the blood.

Cobalamin is made in nature by microbial synthesis–produced by bacteria in the intestinal tracts of animals and stored in their tissues. Some B12 is made during fermentation of foods as well. Cobalamin is the naturally occurring vitamin B12. Cyanocobalamin, as B12 is often known, is actually the commercial variety of B12 and contains a cyanide molecule attached to the cobalt. B12 is not synthesized but, like penicillin, must be grown in bacteria or molds and then processed. Other forms of B12 include hydroxycobalamin (technically, vitamin B12a), aquacobalamin (vitamin B12b), and nitrocobalamin (vitamin B12c).

Sources: Vitamin B12 is found in significant amounts only in the animal protein foods.
B12 is also manufactured by bacteria in the human intestines, but it is not known how much we can naturally absorb and utilize from that source. In general, digestion and absorption must be good for adequate B12 to be obtained. Many laxatives and overuse of antacids can reduce absorption and deplete stores of B12.

Our primary food sources of vitamin B12 include meat, most fish, especially the oily ones (trout, herring, and mackerel), crabs and oysters, eggs (the yolk), and milk products, especially yogurt. Organ meats such as liver, heart, and kidney are particularly high. The vegan–that is, the strict vegetarian who consumes no animal-source foods–is not getting the necessary vitamin B12 from diet (although tempeh, a fermented soybean product, and some sprouts may contain some vitamin B12); thus, vegans will often need an additional supplement (which absorbs well) or periodic injections.

Functions: Although vitamin B12, cobalamin, apparently does not have as many functions
as some of the other B vitamins, it has some very important ones. It is essential for the metabolism of the nerve tissue and necessary for the health of the entire nervous system. It stimulates growth and increases appetite in children. Cobalamin, along with iron, folic acid, copper, protein, and vitamins C and B6, is needed for the formation of normal red blood cells.

Vitamin B12 is the “energy” vitamin, as it often increases the energy level, whether obtained from eating the B12 foods or from supplemental use. There may be several reasons for this. Cobalamin stimulates the utilization of proteins, fats, and carbohydrates. It also helps iron function better in humans and is important for the synthesis of DNA and RNA, as well as for production of choline, another B vitamin, and methionine, an amino acid.

Uses: Vitamin B12 is generally known as the longevity vitamin, possibly because it helps
the energy level and activity of the nervous system of the elderly. B12 injections (the main therapeutic use of this vitamin) have been a common practice of many doctors for the treatment of fatigue, and, in my experience, it works very often. However, it would only be a “cure” when the tiredness is a result of B12 deficiency. There are many reasons for fatigue. As we age, our digestion and absorption are not usually as finely tuned as when we were young, particularly when we eat and live the way most of us late twentieth-century beings do. And vitamin B12, even though it is needed in such small doses, is one of the most difficult vitamins to acquire through diet and to metabolize. The “red vitamin” is the main “antifatigue” vitamin; often given along with folic acid, it helps energy and prevents most anemia, provided there is good iron absorption and hydrochloric acid production.
Medically speaking, it is wise to check patients with fatigue for anemia and to measure vitamin B12 and folic acid levels before embarking on a treatment regimen.

B12, given intramuscularly, usually in doses of 500-1,000 mcg. (0.5-1.0 mg.), is used once, twice, or three times weekly for a period of time to both give energy and, in adults, help with appetite suppression in weight loss programs. These amounts also replenish the vitamin B12 stores. It has a mild diuretic effect as well and may be used premenstrually to diminish water retention symptoms.

In the treatment of pernicious anemia and the earlier symptoms of vitamin B12 deficiency, injections of cobalamin or its variants are usually necessary because most everyone with deficiency has poor absorption. It is difficult to become B12 deficient from diet alone, unless we are on a strict vegan diet for years. In any anemia, really, it is wise to supplement B12, because it helps the red blood cells develop to a point where protein, folic acid, iron, and vitamin C can then complete their maturation so that we can better carry oxygen and energy to all of our cells.

Vitamin B12 will stimulate growth in many malnourished children. In older people, it has helped with energy levels as well as psychological symptoms, including senile psychosis. B12 has also been used to help treat osteoarthritis and osteoporosis and for neuralgias, such as Bell’s palsy, trigeminal neuralgia, or diabetic neuropathy. It has likewise been used in the treatment of hepatitis, shingles, asthma, other allergies, allergic dermatitis, urticaria, eczema, and bursitis. Cobalamin has been used for many other symptoms besides fatigue, including nervousness and irritability, insomnia, memory problems, depression, and poor balance. Vitamin B12 is something to keep in mind when we are not “feeling our oats.”

Deficiency and toxicity: There have been no known toxic effects from megadoses of
vitamin B12. Thousands of times more than the RDA have been injected both intravenously and intramuscularly without any ill consequences. On the contrary, there is often some benefit.

Vitamin B12 deficiency usually results from a combination of factors. Restricted diets, as seen in vegetarians or poor nations, can be very limited in B12. Since the absorption into the body is so finely tuned, depletion and deficiency occur even more commonly from poor digestion and assimilation, or from deficient production of intrinsic factor. That is why it is so important to be aware of B12 and use some sort of supplementation once a deficiency has been diagnosed. Vitamin B12 blood levels, along with folic acid levels, are the most common vitamin tests performed by doctors. As we age, it is more likely that we may become B12 deficient. Also, alcoholics and people with malabsorption or dementia may have low B12 levels. Since the body stores vitamin B12, it may take several years to become deficient with dietary restriction or a decrease in intrinsic factor.

The strict vegetarian has more concern than the average meat- and dairy-eating person. B12 is not found in the vegetable kingdom other than in foods fermented by certain bacteria; thus most fermented foods have some vitamin B12. However, in vegetarians, there is usually a high folic acid intake, and since folic acid and B12 work similarly in the body, a B12 deficiency may be masked for a period of time, and then more pronounced symptoms may occur. If B12 is deficient in an animal eater, then we pretty much know there is a problem in absorption of the vitamin.

Most problems of B12 deficiency affect the blood, energy level, state of mind, and nervous system. Often, subtle symptoms may start with the nervous system. Vitamin B12 nourishes the myelin sheathes over the nerves, which help maintain the normal electrical conductivity through the nerves. Soreness or weakness of the arms or legs, decreased sensory perceptions, difficulty in walking or speaking, neuritis, a diminished reflex response, or limb jerking may result from B12 deficiency. Psychological symptoms may include mood changes with mental slowness may be one of the first symptoms.

With B12 deficiency, the body forms large, immature red blood cells, resulting in a “megaloblastic” anemia. Pernicious anemia refers to the deficiency in blood cells as well as the myriad of psychological and nerve symptoms. The anemia usually generates more fatigue and weakness. Menstrual problems, even amenorrhea (lack of menstrual flow), may also occur in B12-deficient women.

The problems related to the nervous system caused by vitamin B12 deficiency can lead to permanent damage, not correctable by B12 supplementation. This irreversible nerve damage may occur when the B12 deficiency effect on the red blood cells is masked by adequate levels of folic acid, as I mentioned. More severe pernicious anemia can cause a red, sensitive tongue, referred to as “strawberry tongue,” which may even ulcerate, and nerve or brain and spinal cord degeneration, which can cause weakness, numbness, tingling, shooting pains, and sensory hallucinations. Paranoid symptoms may even occur. In the early part of this century, pernicious anemia was often a fatal disease.

Requirements: Vitamin B12 is essential but required only in minute amounts; 3-4 mcg. is
needed in most adults to prevent deficiency, and at least that amount is required by pregnant or lactating women, as well as infants and growing children. From 10-20 mcg. daily is a good insurance level, although certain people may need increased amounts with higher protein intake. Vitamin B12 is often taken in higher doses, 500-1000 mcgs. per day, to relieve fatigue. Injections of B12 in these amounts are used to treat a variety of low-energy and mental symptoms previously described as well as during some weight loss programs. When there is fatigue or anemia, it is a good idea to get the blood level of B12 checked by a doctor. It may lead to a very simple and successful treatment.