Diseases information. Disorders. Treatment.

Okay, another case. Sixty-seven-year-old woman with a new holocranial headache with exposure to cold, tenderness in her scalp and pain upon chewing. That’s a classic history of giant cell arteritis. Scalp pain. Bothers them to touch the scalp. If they chew, they get jaw claudication or tongue claudication, and they are very typically associated with worsening upon exposure to cold. Now fortunately everybody doesn’t walk in here with a little arrow at their superficial temporal artery saying, “Look here.” Many of these people actually don’t have pain or tenderness over their superficial temporal artery. Very few of these people are under 60. It’s rare, rare, rare under that age, but most of them have polymyalgia rheumatica. So they are not well people. They come in, they feel terrible, they are achy. They have this new scalp pain and often it’s worse when they chew. Now you do a sedimentation rate and it’s generally high. There are cases where sed rates are normal. Fortunately they are relatively rare. I generally recommend not just doing a sed rate, but a C-Reactive protein, and a serum viscosity, because what you often find is, as you are treating them, one of these or more than one of these becomes better markers for the activity of their disease. In other words, just counting on sed rates is often not as good. You will find an individual patient where their serum viscosity turns out to be a better marker of how they are doing.
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Now I’ll tell you about another case. This is a case of a 46-year-old woman who came in with the abrupt onset of a severe frontal headache. She actually got better over a few hours. I’ll tell you a secret. Actually she was given sumatriptan, someone gave her sumatriptan and her headache went away so she was sent home, and someone did find that she had a stiff neck in the emergency room. The problem here is that she has a subarachnoid hemorrhage. All that white stuff is blood, she had a huge subarachnoid hemorrhage, responded beautifully to sumatriptan and she went home. Remember, 50% of these people die, 50% mortality, so you can imagine the problems. I will also mention in that, that I saw a patient with meningitis who came in with a fever and a stiff neck. Someone gave them DHE intravenously, it all went away. Sent home, did fine for about three hours and came in moribund. We’ll talk about that in these migraine drugs. But this is a subarachnoid hemorrhage and what makes a history is this: these are people who have the abrupt onset of a headache, terrible headache. It doesn’t come on gradually. It comes on apoplectically. So if someone comes in and says, “I have the abrupt onset of a terrible headache” you think of subarachnoid hemorrhage until proven otherwise. You get a CAT-scan. You don’t do an MRI, you do a CAT-scan and usually the blood will be seen. Occasionally it’s missed, so if you think about that, you do a lumbar puncture. Very, very important. Again, 50% mortality. You don’t want to miss this.
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Subhyaloid hemorrhages are usually seen in the optic nerves. These are puddle-shaped hemorrhages and they are generally within a disc diameter, so you are not going to see them way out here, you are going to see them within a disc diameter.

This is a case of a 31-year-old male who came to see me who had a 15 year history of recurrent right-sided throbbing headaches, that were always preceded by distortions in his left visual field. Now he should have had migraine, and I’ll tell you that the overwhelming majority of people like this have migraine. The only reason we thought anything else is because the headaches were always in the same place and the visual aura was always in the same place, so we did an MRI. This is a big arterial venous malformation in the occipital lobe. Now had he come in and said, “They are almost always on that side, but every once in awhile they switch to the other”, don’t scan them. It’s not worth it. I’ve never seen a person in 20 years of practice who had anything else that imitated migraine, where it shifted, even if it’s 1% or 2% of the time.

Now I’m going to go through some cases.This is a case, sad case, of a 61-year-old male who came in with a six-week history of headaches. The pain awakened him out of sleep and would get better as the day went on. When he would strain at stool, the pain would get worse, and when he would sit up he developed something called visual obscuration. This is a classic brain tumor history. Every neurology book you ever pick up will say, “Brain tumors cause early morning headaches, wake you up out of sleep, get worse if you cough or sneeze.” I think we all learned this in school. Three-quarters of these people with brain tumors had headaches that sounded like tension headaches, and about 9% had migraine-like headaches. About 14% of these people had kind of unclassifiable headaches. But look at this, 8% of all the people with brain tumors had what every neurology book you ever pick up says they are supposed to have. So, so much for that rule.
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The other thing is, it seems that if you have a previous history of headaches and you develop a brain tumor, you are more likely to develop headaches than if you didn’t have a previous history of headaches. It’s very common that what you’ve got now, with your brain tumor, is simply more of what you used to have. What I mean by that is, if you have a history of migraine and you develop a brain tumor, you are likely to develop more, more severe, more persistent migraines than you had before but not necessarily a new headache. If you had cluster headaches, or you had tension headaches, you are more likely to develop more to those, but again, not necessarily a new headache.

Let me talk about another case. This is a case of a 22-year-old woman, came in with new frontal headaches which would increase when she strained at stool and began awakening her out of sleep, and her periods had become abnormal. Now if you look at this lady – she’s a little on the heavy side -if you look at her optic nerve, she has papilledema. What’s wrong with her? Anyone know? Pseudotumor, that’s right. Now we call this idiopathic intracranial hypertension or pseudotumor. Again, most of these are women, most of them are obese, most of them have menstrual irregularities. They have generally non-focal neurological exams, except for papilledema. They have papilledema. Although some don’t, which is spooky. Many of them have a recent weight gain. Some have endocrinopathy’s, and up where I live – I live in the New York area – actually infectious disease is really easy in New York because we actually have only one disease, which is Lyme disease. Everybody either has Lyme disease or thinks they have Lyme disease, and that includes the people who bring them into the office. Actually Lyme disease can cause pseudotumor, so it actually is a fairly important cause.
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So how do you treat these people? Generally we use carbonic and hydrase inhibitors, that’s probably the agent of choice. When I was a resident we used to do lumbar punctures, serially. You need to do one to diagnose these people, you show that their protein is either normal or low, they don’t have cells, their pressure is very, very high. And then we used to do these serial lumbar punctures. We basically used to do one or two a day, every day, until they signed out against medical advice. Which usually didn’t take very long. We came to realize that that is kind butcherous. Furthermore, when you start doing that you actually have a chance of implanting an epidermoid tumor into their spine. So you have to be very careful. If they are getting into trouble, if they have papilledema and they are losing their vision, we recommend doing optic nerve fenestrations and occasionally ventricular shunts.

Ninety percent of persons who seek medical advice for headache have migraine or tension-type headaches, and only 10% of all people have anything else wrong with them. Although there are many types of headaches, the overwhelming majority of people fit into only a very small category of headaches.
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Let’s discuss what doesn’t cause headaches, because these are things which are commonly blamed on causing headaches, which aren’t very important. The first is: refractive errors of the eye. Whether you need glasses or you don’t need glasses is nice, but usually doesn’t have a whole lot to do with why you have chronic recurring headaches. The second is: chronic sinus disease. We know that acute sinusitis causes headaches but that’s easy to recognize, but chronic sinus disease, whether your sinuses are a little thickened or not, generally has very little to do with whether you have, or why you have chronic recurring headaches. Then there are allergies. Allergies are not a very important cause of chronic recurring headaches. They can be a non-specific trigger of headaches in people, particularly migraineurs but by themselves, allergies don’t cause chronic recurring headaches.

The overwhelming majority of headaches are in the eye. People come in and they say, “My eye hurts in here” so they run off to the eye doctor. So the question that then comes up is, if the headache is in the eye, how do you know if you should see your eye doctor? Well, the answer is really simple. One is, you almost never to see your eye doctor because very few causes of headache have anything to do with the eye. The reality is that virtually everything that is sensitive to pain within the brain is supplied by the first division of the trigeminal nerve. V1 fibers are ubiquitous within the anterior middle fossa and even the superior part of the tentorium, so virtually everything that hurts in the head refers pain to the eye. Here’s a rule. All the ocular causes of pain cause changes in the external appearance of the eye. In other words, if you have a red eye, that’s acute glaucoma for example, the first few minutes of acute angle closure glaucoma and very few of these cases are going to be seen in the office, acutely. So basically, if someone comes into the office and they have a white eye and they say the pain is in the eye, forget about their eye doctor.
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Now the IHS, International Headache Society, classified headaches a number of years ago and they put out a very, very long doctrine about hundreds and hundreds and causes of headache. Here’s the Green simplification of the IHS classification, which is probably all it’s worth – one slide. It’s basically worth dividing headaches into primary and secondary headaches. Primary headaches are those in which the headache is the problem, and secondary headaches are those in which the headache is a symptom of another organic neurological disease.

Cyclothymic disorder consists of chronic cyclical episodes of mild depression and symptoms of mild mania.
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DSM IV Diagnostic Criteria

• Many periods of depression and hypomania, occurring for at least 2 years. Depressive episodes do not reach severity of major depression.
• During the 2 year period, the patient has not been symptom-free for more than 2 months at a time.
• During the 2 year period, no episodes of major depression, mania or mixed states were present.
• Symptoms are not accounted for by schizoaffective disorder and do not coexist with schizophrenia, schizophreniform disorder, delusional disorder, or any other psychotic disorder.
• Symptoms are not caused by substance use or general medical condition.
• Symptoms cause significant distress or functional impairment.

Clinical Features of Cyclothymic Disorder

• Symptoms are similar to those of bipolar I disorder, but they are of a lesser magnitude and cycles occur at a faster rate.
• Patients frequently have coexisting substance abuse and one third of patients develop a severe mood disorder (usually bipolar II).
• Occupational and interpersonal impairment is frequent and usually a consequence of hypomanic states.
• Cyclothymic disorder often coexists with borderline personality disorder.

Epidemiology of Cyclothymic Disorder

• The prevalence is 1%, but cyclothymic disorder constitutes 5-10% of psychiatric outpatients.
• The onset occurs between age 15 and 25, and women are affected more than men by a ratio of 3:2.
• Thirty percent of patients have a family history of bipolar disorder.

Differential Diagnosis of Cyclothymic Disorder

Bipolar II Disorder. Patients with bipolar type II disorder exhibit hypomania and episodes of major depression.
Substance-Induced Mood Disorder/Mood Disorder Due to a General Medical Condition. See under dysthymic disorder and bipolar I.
Personality Disorders (antisocial, borderline, histrionic, narcissistic) can be characterized by marked shifts in mood. Personality disorders may coexist with cyclothymic disorder.

Treatment of Cyclothymic Disorder

Mood stabilizers are the treatment of choice, and Lithium is effective in 60% of patients. The clinical use of mood stabilizers is similar to that of bipolar disorder. (Also see “Psychiatric Therapy,” page ).
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Depressive episodes must be treated cautiously because of the risk of precipitating manic symptoms with antidepressants (occurs in 50% of patients). Antidepressants can also increase the rate of cycling. Patients are often treated concurrently with anti-manics and antidepressants.

Patients often require supportive therapy to improve their awareness of their illness and to deal with the functional consequences of their behavior.

Start with a low dose diuretic or a beta blocker, they are equally effective as the new more expensive agents, they are known to provide important benefits to patient’s. I f you want to use long acting calcium channel blockers, there is evidence in the elderly that they are beneficial, it appears as though African Americans and the elderly are more responsive to diuretics so if you have patient’s in that category, a diuretic is the first drug, the contraindications to diuretics are only allergies and gout, and contraindications to beta blockers are listed there. If the patient has diabetes, heart failure or heart attack, refer the patient and I am sure you would all feel comfortable doing that. This is an alga rhythm that the JNC recommends, I won’t go through it, it is in your hand out, it basically says start with a diuretic, if that doesn’t work, you might switch to a beta blocker, or add, if you started with diuretics you can add a beta blocker and if that doesn’t work, then it’s time to refer the patient.
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Followup care once drugs are initiated, one to two months, figure out if the patient is still taking the medicine, whether it’s making him sick, take their blood pressure when standing up to make sure they are not going to fall down in the bathroom and break their hip from hypotension. The lab tests you need to get are small in diuretics, basically it’s basic chemistry panel and calcium because diuretics on rare occasions can elevate calcium and see the patient every two months, once their blood pressure is controlled, you can see them annually. These drug diuretics are very safe and are very effective. There is a list of patient education issues, I can’t over emphasize this enough, if the patient doesn’t know why they are taking medicine, they will stop, because when they saw you, they didn’t feel their blood pressure and there weren’t sick, and now you are asking them to take pills and to do laboratory tests, you need to tell them that the reason to do this is so that they won’t be looking after their grandchildren paralyzed on the left side of their body with a stroke, it’s preventative care.

If you can’t counsel the patient or choose not to, get your nurse to do it. Therapy is life long for hypertension. It is the very rare patient who will get skinny and come off medicines. It happens but it’s rare. Some patient’s think I finished the bottle of my medicine and now I’m okay. Well if you didn’t tell the patient that it’s refillable on a p.r.n. basis for the rest of their lives, they wont’ know that.
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Indications for referral. You can refer if you don’t feel comfortable treating at all but if you feel comfortable treating stage I hypertension with diuretic therapy, I would encourage you to do that. The patient has severe hypertension, end organ disease or some other important medical disease, it is reasonable to refer that patient to a general internist or cardiologist. If they have some evidence of secondary causes, or if you have tired a diuretic and/or a beta blocker and you don’t have their blood pressure below 140 and comfortably below 90, then it is a reasonable thing to refer that patient to somebody who is a little bit more comfortable using the large number of medications which we have for the treatment of hypertension.

I am going to talk to you now about stage I hypertension and what is an indication for beginning drug therapy, all of this presumes that you have measured the blood pressure repeatedly over several months, that you have counseled the patient about life style issues, you have made sure they are not on oral contraceptives, that they are not taking 14 ibuprofen a day, that they are doing reasonably what they can in terms of their dietary salt and alcohol intake. If the patient has a blood pressure of greater than 140/90 for more than a month, and they have something wrong with their heart, kidney or brain, or they have diabetes, they ought to be on a pill. If they have this kind of a blood pressure over this period of time and despite life style counseling, you cannot eliminate their other cardiovascular risk, they ought to be on antihypertensive medication. Other cardiovascular risks we talked about earlier, hyperlipidemia, diabetes, smoking or bad family history. Those are people with stage I hypertension 140/90 or more sustained on multiple readings who ought to be on medicine. IF the patient is officially elderly, 65 and they have sustained elevation of their systolic blood pressure over 150, that is systolic hypertension on multiple readings over at least a month time, the day to show that treating their blood pressure significantly reduces their risk and the last category is very difficult, people with stage I hypertension, they have no other risk factors, they don’t have end organ disease, they have this slightly elevated blood pressure that is slightly into the hypertensive range, it is very difficult to know what to do with those patient’s. Two things are reasonable, it is reasonable to work with them for a year on exercise, losing weight, whatever it is you choose to do and some physicians will choose to treat those patient’s. My own recommendation to you is to talk about it in a straight forward manner with the patient, and get their preferences. Some of our patient’s don’t want to take pills under any circumstances, and under the circumstance, avoidance of medication is a reasonable choice. On the other hand, people are more inclined to take medications they are worried about their blood pressure and when offered the choice, will take the pills, and those people I suggest you ought to give the medication.
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This slide deals with the issue of how low to go when you start treating somebody with high blood pressure, this is from a recent study in the Lancet which deals with that issue and the bottom line is somewhere around 135 to 140 and somewhere around 80 to 85 in terms of the diastolic. Get the blood pressure below 140 and get the diastolic somewhere between 80 and 85, that appears to be the place where risk of cardiovascular events is optimized. You will notice in these slides that reducing the systolic blood pressure to lower levels does not reduce the risk and lowering blood pressure to lower diastolic levels does not reduce the risk, whether or not the risk of a cardiovascular event goes up here, if you get the blood pressure too low is an issue we don’t have time to talk about, remember 135/85 approximately, that is your target.
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If the patient is elderly, this may or may not be possible, it may well be when the patient stands up, they are dizzy, so you may have to compromise, but 140 is a reasonable target, or slightly below for an elderly patient. The pharmaceutical industry has provided us with maybe 300 medicines for high blood pressure, maybe 300, so this is every bit as daunting for you as prescribing oral contraceptives is for me. So I am going to try to distill this into something manageable, these are the categories of antihypertensive agents. Fortunately, you don’t have to know all of that. What this slide shows is that all of the classes of antihypertensive agents, diuretics, alpha blockers, beta blockers, calcium channel blockers, and ACE inhibitors all lower blood pressure at starting doses exactly the same amount, they re all equally effective. Quality of life, impact of these drugs on how the patient perceives their life. Bottom line of this slide, all the same. Patient’s on diuretics do not feel quality of life any worse than patient’s on alpha blockers or beta blockers or calcium channel blockers, so that’s point two. Point three is, the cost, and this is a major differentiator of the classes of antihypertensives, diuretics are down here at the bottom, generic hydrochlorothiazide, $8.00 a month to the patient and if you choose to give the patient what the drug reps are trying to sell you, then you can get the patient to spend $40.00 a month instead of $100.00 a year they will be spending $500.00 or $600.00 a year for the same degree of blood pressure lowering effect and the same impact on their quality of life, and the vast majority of the data that we have about the benefit of antihypertensives is in diuretics and beta blockers. All you need to know is about diuretics and beta blockers.