Drug – bio-affecting and body treating compositions – Preparations characterized by special physical form – Food or edible as carrier for pharmaceutical
Reexamination Certificate
2000-04-27
2002-12-31
Page, Thurman K. (Department: 1615)
Drug, bio-affecting and body treating compositions
Preparations characterized by special physical form
Food or edible as carrier for pharmaceutical
C424S682000
Reexamination Certificate
active
06500450
ABSTRACT:
FIELD OF THE INVENTION
The present invention provides a dietary supplement which supplies a combination of prophylactic and restorative components which assist the body in maintaining normal cerebrovascular tone and reduces the symptoms of migraine headaches.
BACKGROUND OF THE INVENTION
Migraine has been a well-known medical problem for over 5,000 years and represents one of the most investigated types of head pain. Epidemiological research has shown that in the United States, 18% of women and 6% of men suffer from migraine headaches. This extrapolates to approximately 18 million females and 5.6 million males over the age of 12 with this disorder. The prevalence of migraine, according to the Center for Disease Control, has increased 60% from 1981 to 1989. While migraine can occur at any age, 30% of migraine sufferers report their first attack before the age of ten, and the condition is most common in adolescents and young adults. The economic impact of migraine is staggering, with annual cost of the disease estimated at 18 billion dollars.
The basic cause of migraine is still unknown. Although genetics may play a role, with 50 to 70% of migraine sufferers reporting a familial occurrence, no
consistent biochemical or physiological characteristic has yet to be identified in the relatives of those afflicted with the conditions.
There are several pathophysiological views on the origin of migraine. While not mutually exclusive, these views include the a) Êvascular theory, b) central theory, c) neurogenic Inflammation theory and d) platelet theory.
a. Vascular Theory
In 1938, Graham and Wolff, two of the period's most preeminent headache researchers, developed the vascular hypothesis of migraine. They suggested that contraction of the intracranial arteries caused a reduction in blood flow to the visual cortex in the occipital lobe, resulting in the focal neurological symptoms (“aura”) that accompany a migraine episode. As a consequence, the head pain that followed was the result of extra-cranial vasodilatation of the external carotid system, along the nerve compression in the carotid artery wall. These conclusions were based on the observation that the vasoconstricting drug ergotamine tartrate dampened pulsation of the superficial temporal artery (an end branch of the external carotid artery), resulting in migraine pain relief.
Despite the fact that the vascular model has been a dominant concept in migraine pathophysiology, several difficulties arising from this theory have been noted. These include the fact that during a common migraine attack, only minor changes in cerebral blood flow have been noted. Furthermore, oligemia, a phase of reduced blood flow, lasts for several hours longer than the aura. Lastly, the reduced blood flow is not sufficient to induce ischemia, alter neuronal function, and produce the aura phase. As a consequence of these criticisms, the central theory of migraine has been proposed.
b. Central Theory
The central theory suggests that spreading oligemia is the consequence of spreading neuronal depression, which begins as a result of decreased neuronal function in the occipital poles of the brain and progresses forward at a rate of two to three millimeters per minute. The spreading depression involves the depolarization of neurons and has associated with it marked cellular ionic abnormalities. The resulting lowered levels of cellular magnesium increase the likelihood of this type of spreading neuronal depression occurring. This repression of neural function results in a spreading oligemia that can last up to four to six hours. It progresses anteriorly, in a wave-like fashion, over the areas perfused by the middle and posterior cerebral arteries, temporarily impairing cortical vascular functioning. As result, the aura of migraine may be the result of spreading depression, “a phenomenon originating within brain neurons and involving cerebral blood vessels only secondarily.”
c. Neurogenic Inflammation Theory
While the concept of spreading neuronal depression and oligemia may explain the migraine aura, it does not account for ensuing headache. Migraine head pain may be the result of inflammation in the trigeminovascular system (TVS). This theory suggests that the trigeminal nerve fibers innervating cranial vessels are an important component of an elaborate defense network protecting the brain from an actual or perceived insult. Inflammatory neurotransmitters such as substance P, calcitonin gene-related peptide and neurokinin A are released by the fifth cranial nerve. This release signals adjacent meningeal blood vessels to dilate. The resulting neurogenic inflammation sensitizes the neurons and this induces head pain. It is interesting to note that stimulation of the presynaptic serotonin receptor (5HT-1), blocks the release of substance P, thus preventing inflammation and pain.
d. Platelet Theory
Many researchers have felt that serotonin (5HT) is the specific neurochemical cause of migraine. Platelets contain all of the 5HT normally present in blood, and after they aggregate, 5HT is released, resulting in a potent vasoconstricting effect. During migraine attack, platelet 5HT increases in the aura phase and diminishes in the headache phase. Following a migraine attack, there is an increase in urinary 5-hydroxyindolacetic acid (5-HIAA), the main metabolite of serotonin. It is interesting to note that “serotonergic circuits are believed to be involved in modulation of sleep cycles, pain perception, and mood, all important factors in the pathogenesis of migraine.” For example, “a decrease in the firing rate of serotonergic neurons of the midbrain dorsal raphe nucleus occurs with sleep, correlating with the observation that sleep often aborts a migraine attack.”
However, serotonin may not be the only vasoactive chemical involved in the pathogenesis of migraine. Histamine, tyramine, catecholamines (norepinephrine and dopamine), prostaglandin E and free fatty acids may all have important roles to play in migraine pathogenesis.
Existing Treatments—Abortive Therapy
For the migraine sufferer, there are a wide variety of therapeutic approaches both pharmacologic and non-pharmacologic. However, for practical reasons the management of migraine can be divided into a) abortive treatment and b) preventative treatment.
a. Abortive Treatment
An abortive treatment of migraine simply addresses the symptoms. Only pharmacological interventions with analgesics and/or vasoconstrictors are effective for the acute attack. Initial therapy for mild migraine headache is usually aspirin or other nonsteroidal anti-inflammatory agents (e.g. ibuprofen and naproxen sodium). These analgesics, along with sleep in a quiet, dark room, an ice pack on the head and an antiemetic agent, are often sufficient to treat the mild migraine. The use of antiemetic drugs like metoclopramide (Reglan®) is an important variable in determining how effective analgesic action will be. Migraine attacks seem to cause atony and dilation of the stomach along with closure of the pyloric sphincter thereby impairing absorption of the analgesic medications. This decrease in absorption is probably why individuals with migraines generally complain about the lack of effectiveness of this class of drug. Metoclopramide not only helps with the nausea and the headache, but also improves gastrokinetics, correcting the delayed absorption. More potent vasoconstrictors, like ergotamine tartrate, are often combined with nonsteroidal, anti-inflammatory drugs and anti-emetic therapies for moderate to severe migraine attacks. Ergotamine is a potent vasoconstrictor that has been used since the 1920's as an abortive therapy for migraine episodes. While oral therapy can be employed, rectal suppositories of ergotamine are far more effective because it does not interfere with gastrointestinal function. A 1-mg rectal suppository has been shown to provide complete headache relief within three hours of taking the drug in 73% of patients with migraine.
However, despite ergotamine's effectiveness, it must be used intelligently, as frequ
Fubara Blessing
Koppel, Jacobs Patrick & Heybl
Page Thurman K.
Ram Michael J.
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