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How to tell migraine from other types of headache
Migraine and Tension Type Headache are both primary headaches without certain cause, which have a normal physical exam, and tests, and which compromise 99% of all headaches.
One sided, it comes from the Latin word hemicrania which means half of head
Throbbing, pulsatile-can feel your heart beating in your head
Sensitive to light
Sensitive to sound
Severe (5-10) headache
disabling-patient misses work or social activities
Tension Type Headache
non-throbbing, feels like pressure or tight
not associated with nausea , vomiting, or sensitivity to light or sound
is usually mild to moderate (1-5)
patients stay in their life with these headaches, don’t leave work or miss social activities
Migraine aliases: that is, names people call what is usually migraine. Usually these conditions should be treated at onset as if they were a migraine.
Wake up Headache
Let down, holiday, weekend Headache
Recognizing these patterns should help the patient treat at onset, like keeping their triptan and a glass of water at bedside to take if they wake up with a “nocturnal headache.” Migraine should always be treated as quickly as possible because stage 2 where the chemicals come out occurs generally at 20-40 minutes after the start of the migraine and triptans block the release of the chemicals.
Migraine timing cycle: 1) Trigeminal activation, the fifth cranial nerve, the sensory nerve of the face is turned on by the migraine process and pain comes to the eye, forehead, face, sinus, jaw. 2) 20-40 minutes later the neurochemicals CGRD, Neurokinan A, and Substance P are released by the migraine process from ganglia onto the Trigeminal nerve, the arteries, and later onto the Thalamus. 3) At 2 hours the arteries vasodilate and are inflamed. 4) Past 3 hours the thalamus, also known as the pain center of the brain is turned on by the migraine process. Migraine is a chemical inflammatory condition affecting the 5th nerve, the arteries, and thalamus.
The slide below show the 4 phases of the migraine timing cycle.
This slide show the 4 phases of a migraine which starts at 1 with Trigeminal Activation. After 20-40 minutes phase 2 Neuropeptide Release Occurs and the inflammatory chemicals are released. The triptans are 5-HT D and B Receptor inhibitors so they block the release of the neurochemicals if the patient treats early. Then at phase 3, which is about 2 hours into the typical migraine, the Meningeal arteries are vasodilated. Now the trigeminal nerve, the ganglia which release the neuropeptides, and the meningeal arteries are in the skull but not part of the central nervous system. Past 3 hours then the Thalamus is turned on and inflamed and this is the main pain center for the central nervous system. If I drop a brick on my foot, the nerves in the tissues of my foot send a signal up the nerves in my leg, through the spinal cord, and to the thalamus in the brain, where pain is registered. Phase 4 is also called central sensitization and this is the worst and most painful part of a migraine. Then, since migraine is usually an episodic disorder the headache goes away in 4-72 hours and the process stops. Within a day or so the neuropeptides in the brain are metabolized and leave the body through the liver and then the toilet.
However, if one overtreats with certain drugs (caffeine, NSAIDS, Tylenol, pseudoephedrine, triptans, hydrocodone, or butalbital drugs) then episodic migraine may be transformed to Chronic migraine which is defined as >15 migraine days a month. This occurs because the body doesn’t have enough time to eliminate the drugs or the released neuropeptides and they stay in the brain and active this system so that 1-2-3-4 occur continuously, resulting in frequent, oftentimes daily headache. In the 1988 International Classification of headache this syndrome was named “Rebound headache,” but this has been replaced by “Medication Overuse Headache.”
In general all migraine patients should limit caffeine, painkillers, and triptans to only 2 days a week. This is the most that the body can tolerate and get rid of the drug and the neurochemicals without transforming into more frequent headaches.
See drawing below.
Both of Dr. Daniel’s Neurology textbooks: Migraine and Transient Global Amnesia can be found at Amazon.com
Britt Talley Daniel MD
7777 Forest Lane Suite B-220
Dallas, Texas 75230
Bill’s heart pounded so hard and fast that his chest started hurting and he broke out in a sweat. He thought he might be dying and was reduced to terror, suddenly, without cause. Then, almost as quickly as the attack occurred, it faded away. Thinking he had had a heart attack, Bill rushed to an emergency room, where he was examined and told everything was all right. But several days later, he had another attack, and others followed. Bill worried a lot that he was losing control of his life and might even be going crazy. He reported avoidance of social activities, moodiness, poor sleep, and a low level of energy.
Eventually, Bill was diagnosed as having panic disorder. The doctor explained that panic disorder results from a chemical imbalance in the brain that triggers attacks like Bill had been having. The doctor reassured Bill the attacks were not a sign of mental weakness or personal failure. Instead, they’re a sign that the body’s alarm mechanism, which prepares us to fight or run for safety, is out of order. The doctor assured Bill that his intense feelings of losing control or dying could be overwhelming or frightening but that no one had ever died from a panic attack. After a period of treatment with medication and psychological therapy, Bill now lives a more normal life.
Everyday people like Bill are rushed into emergency rooms with symptoms that might indicate anything from heart disease to asthma. About a third of the time, what they are experiencing is a panic attack—an unprovoked explosion of bodily sensations and fear. It has been shown that most panic disorder patients consult physicians other than psychiatrists 10 or more times before their condition is accurately diagnosed.
Panic disorder is characterized by sudden, brief episodes of physical and mental symptoms which, by definition, occur spontaneously or “out of the blue,” to differentiate it from anxiety attacks that have never occurred spontaneously and have always been secondary to a specific reason. For anxiety attacks the patient should have insight or a reason as to why the event occurred. Anxiety would come after a sudden attack by an assailant who wanted to kill you. There would be an evident reason for the symptoms resulting from such an attack. This is not true with panic disorder. Both panic attacks and anxiety turn on the brain’s “fight or flight” mechanism.
The essential feature of a panic attack is a discrete period of intense fear or discomfort that is accompanied by at least 4 of 13 physical or psychological symptoms. The attack has a sudden onset and builds to a peak rapidly, usually in 10 minutes or less. The attack also is often accompanied by a sense of imminent danger or impending doom and an urge to escape. The physical symptoms are: pounding or rapid heart rate, sweating, trembling or shaking, shortness of breath or smothering, choking, chest pain/tightness or discomfort, nausea or abdominal distress, feeling dizzy/lightheaded or faint, numbness or tingling sensations, and chills or hot flushes. The psychological symptoms are: derealization/feeling of detachment, fear of losing control or going crazy, and fear of dying.
The patient may report an intense desire to flee from wherever the attack is occurring. Patients commonly arrive at an emergency room or other medical setting believing that their symptoms represent a heart attack, stroke, or some other catastrophic medical condition. Panic attacks may become associated with a variety of situations in which patients feel an attack is more likely to occur, from which they would be unable to flee or get help quickly if an attack occurred, or in which they might be embarrassed if others should notice they are having an attack.
In reality, a panic attack is often not apparent to an observer, which is why a patient can successfully disguise this condition from others. The development of agoraphobia (fear of being in crowds or around other people) is common and is defined as fear of places or situations in which the patient feels ”trapped.” Patients may not have thought through why they fear or avoid situations when they initially present for treatment. As a result of this fear, they restrict travel or need a companion to enter phobic situations. Common agoraphobic situations are traveling in a car, bus, train, airplane, driving on highways, bridges, tunnels, heavy traffic, being in stores, malls, restaurants, elevators, theaters, church/temple, sitting in a meeting, standing in line, or being home alone.
The cause of panic disorder is still uncertain, but there are theories. A biologic basis is supported by a large volume of research. Certain chemicals may provoke panic attacks, in most panic attack victims, but not in most other people. Some of these chemicals are lactate, caffeine, and cocaine. Medications used to treat panic disorder have been shown to block these attacks. PET scans which reveal the metabolism of the brain show a chemical abnormality in a particular area of the brain of panic patients compared with people who do not have panic disorder. The fact that panic disorder runs in families also suggests a genetic, biologic component to the disease. Psychological theories regarding causes of panic disorder stress the idea that childhood stresses, such as the death of a parent, can predispose a person to phobic reactions. The type of personality that avoids conflict by suppressing feelings and avoiding confrontation is more likely to develop panic disorder. Panic disorder is closely linked to depression, generalized anxiety disorder, tension type headaches, and migraine.
Women get panic disorder about twice as often as men, but some experts suspect that males may be underreported. A large government study revealed that 1% to 2% of the adult population will get panic disorder at some point in their lives. That’s 2-3 million Americans. In addition, another 4% to 5% of adults report having panic attacks and symptoms of agoraphobia who do not qualify for a full diagnosis. The onset of panic disorder has a peak in late adolescene and a second peak in the mid 30s. In general, the treatments now available help reduce or alleviate the symptoms of panic disorder, so that people can lead more normal lives, but do not provide an actual cure.
General treatment of panic disorder includes attention to adequate rest (7-8 hours a night), regular aerobic exercise (20 minutes 3 X a week), a moderate work schedule (workaholism is defined as more that 55hrs/week), and regular vaction time off. Patients with panic disorder should not drink any alcohol at all because it does the same thing the benzodiazepine drugs do, such as Xanax, in that it turns off the part of the brain that starts the fight or flight response. However, because the effect of alcohol only lasts 2 hours, withdrawal symptoms and rebound occur, making panic symptoms worse after the alcohol is metabolized.
Medical treatment consists of using benzodiazepine drugs such as Xanax (alprazolam), taken once a day as XR 1-2 mg, or short acting .25-.5 Xanax which lasts 4 hours and can be dosed as needed or up to 3-4X/day. Also Klonopin (clonazepam) 0.5 mg which lasts 6 hours and can be taken as needed or up to 3/Xday. These drugs act acutely and will shut off the brain now. They often will be given at the start of treatment with an SRI type drug to cover panic symptoms and any nervous or jittery symptoms that may come while the SRI is starting to work. SRI means Serotonin Receptor Inhibitor and refers to a class of drugs that are used to treat depression, generalized anxiety, and panic disorder. They increase the “nice, calming” brain neurochemical, serotonin, but they take several weeks to work. Prozax, Zoloft, Paxil, Effexor, and Celexa all take about 3-4 weeks to kick in. This is called induction. Lexapro can start working in 7-14 days. During the beginning induction period the patient, who is already experiencing panic symptoms, may get more nervous and jittery. It has to be explained to the patient that he has to endure these startup symptoms. Xanax or Klonopin may be given to cover these “getting on the medicine” symptoms and then they may be discontinued in a few weeks when the SRI starts to take effect. Once the SRI starts to work, the Xanax or Klonopin may be tapered and sometimes discontinued. A problem with the use of SRIs is that sometimes the patient has to be tried on several different drugs to get one that fits them—that relieves their symptoms but doesn’t cause side effects. Consider that in this selection and use of the medication the doctor only has clinical guidelines to go by; it’s like treating diabetes without a blood sugar, or hypertension without taking the pressure. Some patients feel like stopping the medication at the beginning, but this should be avoided without calling the office, talking to the doctor, taking the Xanas and Klonopin regularly and daily, and attempting to persevere. In fact toughness and resilence is sometimes required here and the patient will then be rewarded with feeling much better later. You just have to hold on, especially with drugs like Prozac or Zoloft which take three to four weeks to work. Lexapro works faster.
Some doctors use Betablockers like Inderal or Aetenolol or the older antidepressants like Elavil (amitriptyline) or Pamelor (nortryptyline) to treat panic disorder, but the current American Psychiatric Association recommendation is to use an SRI drug. They just work better. Also since Xanax and Klonopin are benzodiazepine drugs and are classified as narcotics and can conceivably be abused, some doctors use Buspar, a nonbenzodiazepine drug which is a minor tranquilizer for anxiety which is not classified as a narcotic. They just don’t work as well as Xanax and Klonopin and in America something like about 60% of patients with anxiety or panic disorder are treated with benzodiazepines.
Treatment options for difficult to treat panic disorder is attention to lifestyle issues, a full dose of an SRI, Xanax 4X/day or Klonopin 3X/day, cognitive psychotherapy with a counselor for 3-6 months, consultation with a psychiatrist, and behavioral therapy. Not every patient needs this full court press type treatment (a basketball term), but some do. Another problem with treatment is that because panic disorder is a psychiatric syndrome, patients commonly just don’t want to admit to themselves and to others that they have such a problem and they resist treatment. They commonly state “I just don’t like to take medication,” as if anyone does. However, once these patients are on therapy for the first time they may feel normal and they may revert back to further attacks when they stop the medication. Sometimes it is difficult for the doctor to know how long to use the medication, but some patients do well with long-term therapy for years. If the patient has only had one or two panic attacks, treatment with a benzodiazepine drugs when the attack occurs may be all that is needed, but if the attacks are more severe, then more aggressive therapy as needed. Maintenance treatment with medication is recommended for at least 12-24 months in most patients, and in some cases, indefinitely.
A last problem with the use of serotonin receptor drugs is that when the patient comes off of them, especially if they are stopped suddenly, they may have withdrawal symptoms. This is worse with short acting drugs like Paxil and not so bad with longer acting drugs like Prozac. The symptoms of discontinuation can include insomnia, vivid dreams, an electric shock sensation, nausea and vomiting, fatigue, myalgia, chills, crying spells, and anxiety/agitation. Simply going back on the medication at the same dose will stop the symptoms. Short acting serotonin receptor inhibitor drugs like Paxil should be tapered slowly by 5 mg a week. In general the physician can consider stopping therapy gradually over 2-6 months.
Criteria for a diagnosis of Panic disorder.
Recurrent unexpected panic attack, defined as a discrete period of intense fear or discomfort, in which four (or more) of the following symptoms developed abruptly and reached a peak within 10 minutes:
(1) palpitations, pounding heart, or accelerated heart rate
(3) trembling or shaking
(4) sensations of shortness of breath or smothering
(5) feeling of choking
(6) chest pain or discomfort
(7) nausea or abdominal distress
(8) feeling dizzy, unsteady, lightheaded, or faint
(9) derealization (feelings of unreality) or depersonalization (being detached from oneself)
(10) fear of losing control or going crazy
(11) fear of dying
(12) paresthesias (numbness or tingling sensations)
(13) chills or hot flushes
At least one of the attacks followed by one month (or more) of one (or more) of the following:
Persistent concern about having additional attacks.
Worried that the implications of the attack or its consequences.
Tab The clinically significant change in behavior related to the attacks
DSM-IV Diagnostic and Statistical Manual of Mental Disorders Fourth Edition
What you should know about panic disorder by Pharmacia
Panic Disorder with or without agoraphobia by Nagy and Charney
Panic Disorder Wayne Katon M.D. N Engl J Med 2006; 354:2360-7
American Psychiatric Association 1400 K St. NW Washington, DC 20005
National Mental Health Association 1021 Prince St. Alexandria, VA 22314
7777 Forest Lane Suite B-220
Dallas, Texas 75230
Approximately 50% of patients with depression may have migraine. The two conditions are said to be co-morbid which means they occur together more likely than by chance. According to the DSM-IV, a person who suffers from major depressive disorder must either have a depressed mood or a loss of interest or pleasure in daily activities consistently for at least a two week period. This mood must represent a change from the person’s normal mood; social, occupational, educational or other important functioning must also be negatively impaired by the change in mood. A depressed mood caused by substances (such as drugs, alcohol, medications) or which is part of a general medical condition is not considered to be major depressive disorder.
The symptoms are not better accounted for by bereavement (i.e., after the loss of a loved one) and the symptoms persist for longer than two months or are characterized by marked functional impairment, morbid preoccupation with worthlessness, suicidal ideation, psychotic symptoms, or psychomotor retardation.
This disorder is characterized by the presence of the majority of these symptoms:
Depressed mood most of the day, nearly every day, as indicated by either subjective report (e.g., feels sad or empty) or observation made by others (e.g., appears tearful). (In children and adolescents, this may be characterized as an irritable mood.)
Markedly diminished interest or pleasure in all, or almost all, activities most of the day, nearly every day
Significant weight loss when not dieting or weight gain (e.g., a change of more than 5 of body weight in a month), or decrease or increase in appetite nearly every day.
Insomnia or hypersomnia nearly every day
Psychomotor agitation or retardation nearly every day
Fatigue or loss of energy nearly every day
Feelings of worthlessness or excessive or inappropriate guilt nearly every day
Diminished ability to think or concentrate, or indecisiveness, nearly every day
Recurrent thoughts of death (not just fear of dying), recurrent suicidal ideation without a specific plan, or a suicide attempt or a specific plan for committing suicide.
Britt Talley Daniel M.D.
7777 Forest Lane Suite B-220
Dallas, Texas 75230
Approximately 40% of persons who have migraine will have stress or anxiety issues. The most common medical diagnosis here is called generalized anxiety disorder which may be abbreviated as GAD. Migraine and GAD are comorbid which means that they occur more likely statistically together than would be expected. Migraine is said to be a genetic problem while anxiety is discussed as familial.
Many persons will say, instead of admitting anxiety, that they have “pressure or stress or worries” but all these are really about the same thing. The DSM-IV is the large standard diagnostic text book from the American Psychiatric Association which lists psychiatric diagnoses and the check list below details how a doctor might diagnose GAD.
DSM-IV Criteria For the Diagnosis of GAD (Generalized Anxiety Disorder)
The patient experiences excessive anxiety and worry
The anxiety is difficult to control
The anxiety is on several subjects
Symptoms occur for more days than not (or > 50% of the time) for the past six months
The patient experiences significant distress or social impairment (withdrawn, sees no one)
There may be at least three ancillary symptoms:
Restlessness/mental tension (time pressure)
Irritability (for intrapersonal relationships)
Muscle tension (tension in neck, shoulders, back, teeth clenching or grinding)
Focus of anxiety/worry is not another disorder (for example, panic disorder)
Not part of a mood disorder, psychotic disorder, or pervasive developmental disorder
Not substance related
DSM-IV= Diagnostic and Statistical Manual of Mental Disorders, fourth edition
Migraine Aggravating Factors/Triggers
Many patients refer to “migraine triggers” but ICDH II differentiates between a migraine trigger which is something that causes an attack within 24 hours, like red wine inducing a migraine, and an “aggravating factor” like stress which builds up over weeks to produce migraine.
Chabriat, et al,[i] wrote in 1999 in Headache on “Precipitating factors of headache. A prospective study in a national control-matched survey in migraineurs and non-migraineurs.” They screened prospective factors in a migraine and non-migraine group of patients who kept a diary for a 3-month period. The most frequent precipitating factors in both groups were:
“fatigue and/or sleep, stress, food and/or drinks, menstruation, heat/cold weather, and infections in both groups.”
Kelman[ii] writing in Cephalalgia in 2007 on “The triggers or precipitants of the acute migraine attack” listed stress at a frequency of 79 % and food at 26.9 %. The table of frequency of individual migraine triggers from his article was:
Hormones (in women) 65.1%
Not eating 57.3%
Sleep disturbance 49.8%
Perfume or odor 43.7%
Neck pain 38.4%
Light (s) 38.1%
Sleeping late 32.0%
Sexual activity 5.2%
Kelman is not going by ICDH-II here which refers to stress as an “aggravating factor”, not a “trigger.” However, his list is interesting and I keep a copy of this article in my office to hand out.
Another observation here is that many patients will focus on the different foods that may aggravate migraine and not recognize stress in their lives which is the most aggravating feature of migraine.
Allodynia with migraine and medication overuse headache
Allodynia comes from the words “allo” which means “other” and “dynia” which means “pain.” Clinically it refers to pain produced by a non-painful stimulus, such as touch. Allodynia is an uncomfortable heightened sensitivity to touch. Normally it doesn’t hurt to touch the head or the brow or the temple, but during the late stages of a migraine or during medication overuse headache, a simple touch to the head or temple may be perceived as painful. This is like a sunburn. Normally if I touch my arm it doesn’t hurt but after a sunburn at the beach, my arm is painful to touch. This is what allodynia is like.
Allodynia can be divided into: tactile allodynia-pain from touch or light pressure like a belt or bra strap, mechanical allodynia-pain from motion across the skin such as light massage or the touch of fabric, and thermal allodynia-pain from heat or cold that makes the limbs feel needle like, sharp pain.
The pain of allodynia can be provoked by combing or brushing the hair, shaving, showering, wearing glasses, or earrings. The pressure of a strand of hair may feel like the jab of a hot knife. Allodynia is the migraine patient who notes on the third day of headache suffering that it hurts her to brush her hair or lay her head on the pillow.
Allodynia occurs mostly in long duration episodic migraine attacks or in patients transformed to medication overuse headache by overtreatment of headache with analgesics. The duration of migraine is 4-72 hours, as defined by the International Classification of Headache 2004. Migraine is generally an episodic, paroxysmal disorder occurring at most 2 times a week. One can easily see by doing simple math that multiplying 72 hours or 3 days by 2 equals 6 days. This is why periodic migraine rarely occurs more than twice a week. Daily headache or headache 3 or 4 days a week is usually Chronic Daily Headache (CDH), a syndrome defined as >15 headache days a week. About 70% of persons with CDH have a common headache syndrome from overtreating with analgesics, caffeine, or triptans called Medication Overuse Headache. Also read my article on the subject of Medication Overuse Headache on this blog.
An attack of migraine has 4 stages: 1) trigeminal activation, 2) neurochemical release, 3) arterial vasodilatation, 4) central sensitization of the thalamus in the brain. In general patients with an attack of migraine are at stage 3 in two hours and after two hours they are in stage 4. Thus, patients with long-duration (headaches lasting more than several hours) episodic migraine attacks spend most of the time in stage 4 central sensitization. The general thinking is that all patients with medication overuse headache are continuously in stage 4 central sensitization. Both of these circumstances can produce allodynia.
With episodic migraine the allodynia clears when the headache ends and the offending neurochemicals are metabolized and excreted. The same thing occurs during treatment of medication overuse headache when the patient is detoxed off of analgesics, caffeine, or triptans. In time the offending neurochemicals are metabolized and consequently the headache clears.
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Betablockers are “Vasonormalizers” which prevent dilation and constriction of arteries. Adrenaline is made in two varieties: Alpha—which works on the lungs, and Beta—which works on arteries, thus, the name betablocker. The archetype betablocker drug is Inderal, known generically as propanolol. This drug works to block some of the effects of adrenaline on arteries. Other Betablockers that may be used are: Corgard (naldolol) and Tenormin (atenolol).
Inderal has been approved by the Federal Drug Administration for the treatment of a large variety of medical problems which includes: Migraine, Benign Essential Tremor or Familial Tremor, Hypertension, Angina (the chest pain heart patients with coronary artery disease get), Cardiac Arrhythmias.
Inderal comes in a short term (4 hour lasting) dose usally given 3 or 4 times a day or in LA (long acting-24 hour) once a day form. Common doses are 80-320 mg/day. For younger patients with migraine or tremor the dose may be discontinued safely at a low dose such as 80 mg/day, while older patients with heart disease and higher doses should have the dose tapered slowly.
Inderal is usually well tolerated and has few side effects, although like all drugs it has two pages of small print listing possible side effects. One potential side effect is that a small number of patients may develop the so called “Inderal tired syndrome” after they start the drug, usually in the first week. If this symptom develops, then the drug should be stopped and another betablocker selected. Betablockers may worsen depression or asthma and should be used with caution with these medical conditions
Duration of therapy
How long the drug has to be given is not known at the beginning and depends on the clinical indications. For tremor Inderal is usually given long term for years or life. For migraine I commonly encourage the patient to consider using the drug for 3-6 months at first and then reassess on follow up. Daily preventive drugs like betablockers may be offered to migraine patients if they are experiencing at least 3-4 migraines a month. The general effectiveness for migraine prevention is reduction in number of migraines by 50%. Many patients are able to get off the drug if their headache diaries show that their number of events is low, although some patients with bad migraine should continue.
Inderal (propranalol) would be a good preventive drug choice for a patient with both migraine and essential tremor, but a poor choice for the patient with migraine and depression.
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RISK FACTORS FOR ATHEROSCLEROSIS
From the American Heart Association
1) Genetics – your own family’s history of heart disease/stroke.
3) Cholesterol Level – less than 200 in general; also LDL cholesterol, homocysteine, fibrinogen, low-density lipoprotein, and C reactive protein.
4) Hypertension-a blood pressure over 130 systolic or 90 diastolic.
7) Level of Activity – all persons should do 20 minutes of Aerobic Exercise three times a week. Aerobic exercise is defined by the heart rate. There are published tables for desired heart rates for different ages of life. If you do an activity that gets your heart rate in the target area, then that is aerobic exercise. Common types of aerobic exercise are jogging, Jane Fonda type exercises, a rowing machine, treadmill, stepper, cardioglide machine, cross country skier machine. Walking, playing golf or tennis, even racquetball are not aerobic exercise, because the heart rate doesn’t get high enough.
Athero (fat), sclerosis (hardening) means hardening of the arteries and is a generalized disease process affecting all the major arteries in the body, mainly the heart and arteries to the brain. Atherosclerosis is a complex, multifactorial disease process with genetic and environmental factors. In the United States the number one cause of death over age 50 is heart disease from atherosclerosis. The number three cause of death is stroke, again from atherosclerosis. There are no “chemical roto-rooters” to open up arteries. Surgeons and cardiologists may do this in selected cases if the disease process is focally present in one area, like the carotid artery going to the brain, or a coronary artery supplying the heart. The idea is to try to live a type of life that reduces the risk factors of atherosclerosis–quit smoking, lose weight, treat hypertension, care for your diabetes, watch your cholesterol, and exercise aerobically.
A research report studying 40,000 patients for 40 years showed that persons who exercised lived two years longer than persons who did not. This was at Framingham, Massachusetts, the oldest heart disease study group in America.
Exercise may be considered to be like a drug. It promotes the relaxing response, helps reduce tension, and increases endorphins which are internal brain chemicals that decrease pain. Exercise may help migraine, tension type headache, anxiety, panic disorder, insomnia, and depression.
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Tips for Sleeping Well
Items 1 through 4 are called normal sleep hygiene and should be done by everyone.
1. Establish a daily sleep/wake schedule. This means keeping a consistent time each day for waking up the morning and going to bed each night. Try to stay within 30-60 minutes of these times every day. This includes through the weekend, holidays, and vacations. In general allow AT LEAST 7 -8 hours of sleep each night. As we age, we need less sleep, so someone in his eighties may need only 6 1/2 hours, while teenagers may well need 9-10 hours.
2. Be careful with naps. It’s okay in general to take a short nap after lunch, a siesta, but avoid a long nap. If you can’t do this on your own, then set an alarm for a brief 15-30 minute nap. If you have trouble falling asleep at night when you have napped earlier during the day, then eliminate the nap. Just lie down and rest for 10-15 minutes instead during the day. If you are the type who “never learned to rest” then, LEARN. The relaxing response can be taught at any age.
3. Be careful with caffeine and pseudoephedrine, both of which promote alertness. Caffeine lasts 8 hours. If you go to sleep at night at 11 pm, then don’t drink any caffeine any later than 3 pm. Pseudoephedrine is in a lot of over the counter sinus or cold medicines-such as Sudafed, Claritin D, or Tylenol Sinus.
4. Regular physical exercise promotes sleeping well. The American Heart Association recommends that every body exercise aerobically for 20 minutes 3 times a week to decrease the risk of atherosclerosis. As a physician I rarely see patients who do manual labor-carpenters, maids-who have trouble sleeping. Exercise promotes the relaxing response. A warning here is that some persons get too jived up after exercise to go to sleep. They should exercise earlier during the day. Exercise also induces endorphins, brain neurochemicals that reduce pain and promote calming.
5. A low volume of a high calorie carbohydrate just before bedtime promotes sleep. I’m talking about something like the proverbial “warm glass of milk.” This has been studied scientifically and shown to work. You have to be careful here with the calories and cholesterol.
6. It’s okay to get out of bed and go to another room for awhile, if you can’t fall asleep when you first try. Then you may read , preferably something not too interesting , technical, or work related, for 10-15 minutes. However, watching TV or doing housework are not good options. They’re too stimulating.
7. Home remedies, vitamins, food supplements, and over the counter sleeping pills don’t usually work for long term sleeping problems. Therefore avoid them. This includes Benadryl which is in Tylenol PM, other antihistamines, and Chloral Hydrate. Melatonin is a drug that may rarely work for small subset of patients with insomnia. Unfortunately, it doesn’t work for everyone. A dose of 3-12 mg of melatonin may be tried.
8. Ambien is a class 4 narcotic, hypnotic sleeping pill with abuse potential that has been approved for chronic use. Some patients are drowsy after using it and may be up at night and perform automatic funtctions, like raiding the refrigerator. Other hypnotics are Restoril and Dalmane. Rozerem is a non narcotic drug that works on the melatonin brain stem system.
9. Alcohol and minor tranquilizers (the Benzodiazepine drugs-Valium, Xanax, Ativan)-don’t work that well either because they don’t last all night and are not good long term options.
10. The majority of patients who have chronic sleeping problems also have psychological reactions or conditions that interfere with sleep. Work directed toward resolving conflicts (psychotherapy, cognitive behavioral therapy) may be helpful. Sleep lab information states that half of patients in America with insomnia are anxious and a quarter of them are depressed. These are the most common causes of trouble sleeping.
11. The older antidepressant medications are, in general, safe for chronic sleep disorders. Examples here would be: Elavil (amitriptyline), Desyrel (trazodone), Tofranil, or Pamelor. All of these drugs have a sedating quality which will allow normal physiological sleep. They are not addictive or habituating. They commonly have mild side effects of a dry mouth which improves with therapy. These are the drugs that may be used for long term sleep disorders. Trazodone comes as a 50 mg tablet and this works well for the majority of patients with trouble sleeping. However, if this dose is too high the patient should break it in half and take 25 mg. A maximum of 150 mg/night may be used. If the patient doesn’t sleep all night on 50 mg then he should increase the dose by 25 mg /night per week until he sleeps all night. The same approach may be used with amitriptyline where the dose may be started at 10 mg and can be just adjusted upward by 10 mg/night to about 50 mg until the patient sleeps all night.
12. Sleeping is an important issue with migraine because too much or too little sleep may make it worse. These sleep tips will help treat migraine in a sense.