Every time I go all introspective and a little low after a hypo period I start to blog. I start to read more about my condition. I try to find answers. I try to find a cure.
Every time. I am so much of a broken record it’s embarrassing.
The funny thing is that it seems to happen at the same time every year.
I have a happy hypo extremely productive spring. I feel on top of the world. Then I start to flag by the end of summer. My migraines kick in and then come autumn I have a little crash. That if not dealt with by resting causes a major problem come winter. I have a tendency to need to hibernate.
Another interesting article.
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Are Migraines and Bipolar Disorder Related?
Are Migraines and Bipolar Disorder Related?
August 01, 2002 | Bipolar Disorder, Schizophrenia, Comorbidity In Psychiatry, Bipolar II Disorder, Major Depressive Disorder
By Ole Bernt Fasmer, MD and Ketil Joachim Oedegaard, MD
Migraine is characterized by episodes of headache with qualities such as unilateral location, throbbing pain and aggravation by routine physical activity. Additional symptoms include nausea, photophobia and phonophobia. Some patients have aura symptoms, usually visual, before the headache phase (Davidoff, 1995). Prodromal and accompanying symptoms of migraine attacks often are psychiatric in nature, such as depression, elation, irritability, anxiety, overactivity, difficulty thinking, anorexia or increased appetite. In some patients, an organic mental syndrome can be part of a migraine attack (Davidoff, 1995). In other patients, an acute psychotic condition is the dominating clinical feature. This presentation, with paranoid delusions, hallucinations and anxiety, has been described in families with hemiplegic migraine (Spranger et al., 1999). Migraine is, therefore, an important differential diagnosis in relation to episodic phenomena with a mixture of somatic and psychiatric symptoms. In addition, psychosocial stress is the most common precipitating factor for a migraine attack (Davidoff, 1995).
Migraine is an organic disorder with a clear genetic background, even if environmental factors also are important both etiologically and in the precipitation of individual attacks. It is now fairly well-established that migraine has a primary neuronal basis, although blood vessels also are involved in the series of events that constitute a migraine attack (Aurora and Welch, 2000).
The prevalence is usually between 10% and 15% in epidemiological studies, and migraine is more common in women than in men (Silberstein and Lipton, 1993). Neurochemical disturbances are thought primarily to involve the serotonergic (Silberstein, 1994) and the dopaminergic systems (Hargreaves and Shepheard, 1999). Drugs acting on serotonergic neurons or receptors may induce migraine headaches, and migraine patients are more sensitive than others to dopaminergic stimulation. In familial hemiplegic migraine, dysfunctional neuronal calcium channels have been found (Hargreaves and Shepheard, 1999).
Comorbidity of Migraine and Affective Disorders
A total of 102 patients, 79% of them inpatients between 18 and 65 years old, with major affective disorders were interviewed in two studies (Fasmer, 2001; Fasmer and Oedegaard, 2002). In the first study, we interviewed 62 consecutively admitted patients with major affective disorders and examined the frequency of migraine in patients with unipolar and bipolar disorders (BD) (Fasmer, 2001). In the second study, we recruited an additional 40 patients; and in the entire group of patients (n=102), we looked more closely at the clinical characteristics of the patients with migraine compared to those without migraine (Fasmer and Oedegaard, 2001). We used a clinical interview based on criteria from the DSM-IV, supplemented with Akiskal’s criteria for affective temperaments (Akiskal and Akiskal, 1992; Akiskal and Mallya, 1987). Bipolar I disorder (BDI) was diagnosed according to DSM-IV, while bipolar II disorder (BDII) encompassed patients with either discrete hypomanic episodes or an affective temperament (cyclothymic or hyperthymic), in addition to major depressive episodes. We employed the criteria of the International Headache Society (1988) to diagnose migraine.
In both studies, we found migraine to be a common comorbid disorder in patients with unipolar depressive disorder or BD, affecting approximately half of the patients in each group. However, most of the patients we interviewed did not present migraine headaches as a prominent complaint, and often a history of migraine was not noted in the hospital records. The most interesting finding was a substantial difference between patients with BDI and BDII, with migraine being clearly more prevalent in the BDII than in the BDI group. In our second study, 82% of the patients with BDII had migraine, compared to 27% of the patients with BDI (Figure). There is much evidence, including our own, indicating that patients with BDI and BDII represent two different nosological conditions (Coryell, 1996). Our results are similar to those of Endicott (1989), who found, among patients with major affective disorders, the highest frequency of migraine (51%) in patients having characteristics similar to patients with BDII as defined in the present study.
The most noteworthy findings concerning the clinical characteristics were that patients with migraine had a higher frequency of affective temperaments (47% versus 22% in patients without migraine) and a higher number of anxiety disorders. They were more likely to have panic disorder (51% versus 24%) and agoraphobia (58% versus 27%) than the patients without migraine. Symptoms during depressive episodes were similar, except that the migraine patients reported irritability and suspiciousness with increased frequency.
In two epidemiological studies, one from Zurich, Switzerland, (Merikangas et al., 1990) and one from Detroit (Breslau and Davis, 1992), a clear relationship between migraine and major affective disorders has been found (Breslau et al., 1994). In the Zurich study, people with migraine had a threefold-increased one-year prevalence of bipolar spectrum disorders (9% versus 3%), a nonsignificant increase in manic episodes and a twofold-increased prevalence of major depression (15% versus 7%).
Although these results cannot be directly compared to ours, they show that the association of migraine and affective disorders is not only found in such a selected group as we have studied. In these epidemiological studies, people with migraine also had an increased frequency of anxiety disorders. In the study by Breslau and Davis (1992), the frequency was doubled, compared to people without migraine, and the association was especially strong for panic disorder, with a sixfold increase. In contrast to these findings in patients with affective disorders, a study of patients with schizophrenia found no increased frequency of migraine (Kuritzky et al., 1999).
In our second study, the age of onset of the first anxiety disorder (most often a specific phobia) for patients with migraine was 15 years of age. This was earlier than the onset of migraine (21 years), which again was earlier than the onset of the first depressive episode (26 years). The first hypomanic episode occurred at age 28 (Figure). These chronological relationships are in agreement with previous studies. The high prevalence of anxiety disorders in patients with major affective disorders and comorbid migraine supports the hypothesis that there is a syndromal relationship between migraine, anxiety and depression (Merikangas et al., 1990). We would add that bipolar features should be included as part of this syndrome, and possibly the presence of migraine may be used to delineate a distinct subgroup of the major affective disorders.
Treatment Considerations for Both Disorders
To our knowledge, there are no studies that have specifically examined responses to drug treatment in patients with major affective disorders and comorbid migraine. Guidelines for pharmacological treatment must, therefore, be based on data from the neurological literature combined with data from the treatment of major depressive disorder, BDII and panic disorder.
Concerning antidepressants, amitriptyline (Elavil, Endep) is the drug that has been best studied in the prophylactic treatment of migraine and has been shown to reduce the frequency of attacks by 40%. This effect seems to be unrelated to its effect on depression (Ramadan et al., 1997). Selective serotonin reuptake inhibitors are less effective than either amitriptyline or propanolol (Inderal) (Silberstein, 1998).
In open studies, lithium has been shown to be useful in some patients with migraine (Medina and Diamond, 1981), however, others have reported worsening of migraine with lithium (Peatfield and Rose, 1981). Carbamazepine (Tegretol) does not seem to have any effect in patients with migraine (Post and Silberstein, 1994).
Several studies, both open and controlled, have shown that valproate (Depakene) has prophylactic effect in migraine, reducing the number of attacks, duration of headache and intensity of pain (Silberstein, 1996). Valproate thus has effect on the three main symptom groups in patients with migraine and comorbid affective disorders: headaches, mood instability and panic attacks (Freeman et al., 2002).
In the acute treatment of migraine, triptans, which exert their effect by a combination of vasoconstriction and decreased release of inflammatory mediators (Blier and Bergeron, 1995), are usually employed. The oldest and best-studied is sumatriptan (Imitrex). Although sumatriptan apparently has limited ability to penetrate the blood-brain barrier (Millson et al., 2000), it has been implicated in adverse events resembling the serotonin syndrome, when combined with centrally acting serotonergic drugs. However, the number of reported cases is small, and most patients seem to tolerate this combination without problems (Gardner and Lynd, 1998).
It is theoretically possible that the risk of depressive illness may be increased by the use of triptans, especially the newer ones which have enhanced lipophilicity, but this could not be confirmed in a recent study of consulting rates in general practice (Millson et al., 2000).
This research has been supported financially by the legacy of Gerda Meyer Nyquist Gulbrandson and Gerdt Meyer Nyquist.
Dr. Fasmer is associate professor of medicine in the department of psychiatry at University of Bergen and senior consultant at Haukeland Hospital, Bergen, Norway.
Dr. Oedegaard is research fellow in the department of psychiatry at University of Bergen and senior consultant at Haukeland Hospital, Bergen.
Akiskal HS, Akiskal K (1992), Cyclothymic, hyperthymic, and depressive temperaments as subaffective variants of mood disorders. In: American Psychiatric Press Review of Psychiatry, Vol. 11, Tasman A, Riba MB, eds. Washington, D.C.: American Psychiatric Press, pp43-62.
Akiskal HS, Mallya G (1987), Criteria for the “soft” bipolar spectrum: treatment implications. Psychopharmacol Bull 23(1):68-73.
Aurora SK, Welch KM (2000), Migraine: imaging the aura. Curr Opin Neurol 13(3):273-276.
Blier P, Bergeron R (1995), The safety of concomitant use of sumatriptan and antidepressant treatments. J Clin Psychopharmacol 15(2):106-109.
Breslau N, Davis GC (1992), Migraine, major depression and panic disorder: a prospective epidemiologic study of young adults. Cephalalgia 12(2):85-90 [see comment].
Breslau N, Merikangas K, Bowden CL (1994), Comorbidity of migraine and major affective disorders. Neurology 44 (10 suppl 7):S17-S22.
Coryell W (1996), Bipolar II disorder: a progress report. J Affect Disord 41(3):159-162.
Davidoff RA (1995), Migraine: Manifestations, Pathogenesis, and Management. Philadelphia: F. A. Davis.
Endicott NA (1989), Psychophysiological correlates of ‘bipolarity.’ J Affect Disord 17(1):47-56.
Fasmer OB (2001), The prevalence of migraine in patients with bipolar and unipolar affective disorders. Cephalalgia 21(9):894-899.
Fasmer OB, Oedegaard KJ (2001), Clinical characteristics of patients with major affective disorders and comorbid migraine. World Journal of Biological Psychiatry 2(3):149-155.
Freeman MP, Freeman SA, McElroy SL (2002), The comorbidity of bipolar and anxiety disorders: prevalence, psychobiology, and treatment issues. J Affect Disord 68(1):1-23.
Gardner DM, Lynd LD (1998), Sumatriptan contraindications and the serotonin syndrome. Ann Pharmacother 32(1):33-38.
Hargreaves RJ, Shepheard SL (1999), Pathophysiology of migraine-new insights. Can J Neurol Sci 26(suppl 3):S12-S19.
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Medina JL, Diamond S (1981), Cyclical migraine. Arch Neurol 38(6):343-344.
Merikangas KR, Angst J, Isler H (1990), Migraine and psychopathology. Results of the Zurich cohort study of young adults. Arch Gen Psychiatry 47(9):849-853.
Millson D, Frischer M, Croft P, Goadsby PJ (2000), Are triptans with enhanced lipophilicity used for the acute treatment of migraine associated with an increased consulting rate for depressive illness? Cephalalgia 20(8):732-737.
Peatfield RC, Rose FC (1981), Exacerbation of migraine by treatment with lithium. Headache 21(4):140-142.
Post RM, Silberstein SD (1994), Shared mechanisms in affective illness, epilepsy, and migraine. Neurology 44(10 suppl 7):S37-S47.
Ramadan NM, Schultz LL, Gilkey SJ (1997), Migraine prophylactic drugs: proof of efficacy, utilization and cost. Cephalalgia 17(2):73-80.
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James Phelps, MD, is Director of the Mood Disorders Program at Samaritan Mental Health in Corvallis, Ore. His Web site, PsychEducation.org, gathers no information on visitors and produces no income for him or others. He is the author of Why Am I Still Depressed? Recognizing and Managing the Ups and Downs of Bipolar II and Soft Bipolar Disorder (New York: McGraw-Hill; 2006), from which he receives royalties. Dr Phelps stopped accepting honoraria from pharmaceutical companies in 2008.
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This article is very interesting.
NEWS & PERSPECTIVE › MULTISPECIALTY
Borderline Personality Disorder and Migraine
John Rothrock MD, Ivan Lopez MD, Richard Zweilfer MD, Diane Andress-Rothrock BA, Renay Drinkard C-NP, Naomi WaltersDisclosures
In our clinic-based study of patients with migraine, coexisting BPD was associated with female gender, more pervasive headache, greater migraine-related disability, a higher prevalence of MOH, more unscheduled visits for acute headache treatment, a higher prevalence of moderate-to-severe depression, and a lower likelihood of responding to pharmacologic treatment intended for migraine prophylaxis. Many of these findings previously have been reported, albeit not necessarily in the same context. As examples, others have reported that a significant majority of BPD patients are female, and severe headache was noted to be highly prevalent in one study of BPD patients actively receiving psychiatric therapy.[3,9] A number of investigators have reported a high prevalence of substance abuse in psychiatric patients with BPD, and in a study of BPD patients with migraine it consequently should not be surprising to find-as we did-a disproportionately high prevalence of overuse of symptomatic medications.[10,11] Finally, there exist data indicating that psychiatric comorbidity of various types is higher in patients with TM than in those with EM, and our data suggest that BPD specifically may be associated with more pervasive and disabling headache.
What advantages could result from early identification of BPD in a headache clinic population? For one, the treating clinician then may anticipate the eventual emergence of behavior disruptive to the therapeutic alliance and so implement proactively strategies intended to establish clear boundaries and minimize that behavior (eg, treatment contracts). For another, when BPD is present, the treating clinician may wish to refer the patient for psychiatric comanagement; psychotherapy combined with psychopharmacologic treatment may impact BPD positively. As our own data reflect, depression is comorbid with BPD, and prescription of an antidepressant may be appropriate for those patients with true depression of moderate-to-severe proportions. Finally, identification of BPD should guide the clinician to avoid the prescription of certain medications; given the high prevalence of benzodiazepine abuse in the BPD population, this class of agents is at least relatively contraindicated, and-aside from a similar concern regarding abuse potential-opioid use may aggravate the behavioral symptomatology associated with BPD.[10,16]
The MSI-BPD is a self-report screening instrument for detection of BPD that has exhibited high sensitivity and specificity when administered to individuals with a psychiatric treatment history recruited via a newspaper advertisement and posters placed around a hospital campus; its diagnostic efficiency was highest in patients 25 years old or younger. In our study the MSI-BPD was not effective in identifying BPD in patients previously diagnosed as having that disorder. Interestingly, even those of our BPD patients who “passed” the MSI-BPD undetected were highly likely to record scores on the QIDS-SR that correlated with moderate-to-severe depression. Although the relatively high age of our BPD population (32.9 years) may have reduced the efficiency of the MSI-BPD, it seems unlikely that this factor by itself accounted for the instrument’s low sensitivity. Because the instrument currently regarded by many as the “gold standard” for BPD diagnosis-ie, the Structured Clinical Interview for DSM-IV Axis II Personality Disorders, or SCID-II-had not been administered uniformly to all patients with presumed BPD, that diagnosis may have been inaccurate in at least a portion of our Group 1 subjects. While it is also conceivable that the instrument’s insensitivity may have reflected some qualitative difference in the psychiatric symptomatology experienced by our patients relative to those tested in the validation study by Zanarini et al (eg, our patients were “higher functioning”), it may be that the clinical setting within which the instrument was administered-a headache clinic as opposed to a specific psychiatric clinical trial restricted to subjects with BPD and a history of psychiatric treatment-was the factor most decisively influencing outcome. If true, this last may have implications for other screening instruments used to detect psychiatric disease, ie, does the efficiency of these instruments vary according to the clinical setting within which they are administered?
In summary, our data suggest the following:
In the headache clinic populations with migraine, BPD is associated with
more pervasive headache
greater migraine-related disability
a high prevalence of self-reported depression
a higher prevalence of presumed MOH
more unscheduled visits for acute headache treatment
a lower likelihood of responding to a chronic migraine treatment strategy, and
The MSI-BPD may not be diagnostically sensitive in the headache clinic setting.
4 of 4
Robin Williams’ Suicide Had Nothing to Do With Demons
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Dr. John Rothrock, University of Alabama at Birmingham, RWUH M226, 1530 3rd Ave. South, Birmingham, AL 35294-3280.
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Headache. 2007;47(1):22-26. © 2007 Blackwell Publishing
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I’m having more of my do’s. I’ve had two migraine/ dizzy spells so far this week and have had to take a week off work to attempt recuperation.
I feel unreal. I’ve tried sleeping tablets again, perhaps I’m just exhausted? Uhuh the vicious cycle of bipolar strikes again. My daily moods are under control but not the condition overall. How am I supposed to hold down a job if for 6 months I’m ok/hypo/high functioning and 6 months after I need to rest? How does one cope with the bpd bipolar battle going on inside my head? I could cry. I probably will. Bleugh.
Every year the same….
Yet again I’m feeling let down, rejected, criticised, useless, overlooked, unappreciated and victimised by my boss. The one who I once held in such high esteem. She does take out her stresses on her staff, but it seems too personal. It must be my bpd, cos its such a recurring pattern following a hypomanic episode, yet again I’m thinking about not being here. I’m about to slide. But I can’t live like this. I can’t keep having months off work. I know my mat leave masked some of this pattern, but signs are/were there. How do I go on, I need a wage.
I’m exhausted of it all.
Laughter is by far the greatest medicine. I feel rather hyper. Have done for a while. But I LIKE IT!!!! I feel like ME. I am invincible at the moment. Let’s hope it stays that way, I mean why not. I like silly. I like singing. I feel great. Live love and laugh. I feel radiant like a shining positive beacon of sarahness.