Search PubMed⌕ Search
Home/Archive/PubMed

PubMed · 11264694

Transitional interpersonality thunderclap headache.

D E Jacome
View original source ↗Export metadata ↓

Abstract

OBJECTIVE: To report a patient with multiple personality disorder who experienced severe acute headaches without warnings, solely during the transition between her host personality and her pain-prone personality. BACKGROUND: The initial detailed description of headache in multiple personality disorder was made by Packard and Brown and published in this journal 15 years ago. METHODS: Clinical history, neurologic examination, electroencephalogram, and brain magnetic resonance imaging. RESULTS: A 54-year-old Holocaust survivor with an established diagnosis of multiple personality disorder had recurrent, excruciating, acute ("thunderclap") headaches only when switching between her domineering personality and her pain-prone personality, who suffered from chronic back pain. None of her personalities otherwise suffer from headaches. Electroencephalogram and brain magnetic resonance imaging were normal. CONCLUSION: This is an independent and current confirmation of the existence of transitional headaches in a patient with multiple personality disorder. They may occur as an isolated event during the switch process and have features of benign thunderclap headache.

Explore related subjects

Acute DiseaseDissociative Identity DisorderFemaleHeadache DisordersHumansMiddle AgedRecurrenceSeverity of Illness IndexCase ReportsJournal Article

Keep this discovery

Explore connections, maps & timelines

BibTeXRIS

D E Jacome. 2001. Transitional interpersonality thunderclap headache.. https://doi.org/10.1046/j.1526-4610.2001.111006317.x

Cite the original work for its findings. Save a collection to share your selection of sources.

KEEP EXPLORING

Related citations

PubMed2002

Urticaria.

Explore the source record for details and available documents.

Acute Disease↗
PubMed2001

Early IFN-gamma production is related to the presence of interleukin (IL)-18 and the absence of IL-13 in experimental Trypanosoma cruzi infections.

Gamma-interferon (IFN-gamma) production, the hallmark of the Th1 immune response, has been shown to play a central role in the resistance to Trypanosoma cruzi infections, in particular when produced in the very early acute infection. BALB/c mice infected with T. cruzi, Tulahuén strain, reach high parasitemias during the acute phase, and their spleen cells release IFN-gamma in the second week of the infection, while those of the resistant C3H strain produce the cytokine earlier, at 2 days post-infection (pi). We studied in the spleen cells supernatants of infected BALB/c and C3H mice, the spontaneous production of cytokines involved in the induction, interleukin (IL)-18 and IL-12 p70, as well as in the downregulation, IL-13 and IL-10, of the Th1 immune response. We found that, at 2 days pi, only C3H mice produced IL-18, while IL-12 p70 was detected in both mouse strains. Moreover, at this time pi splenocytes from BALB/c mice spontaneously produced high amounts of IL-13. At 14 days pi, despite the increased levels of IL-13 and IL-10 detected in C3H mice, they still showed high concentrations of IL-18 and IL-12 p70. In contrast, spleen cells from BALB/c mice did not secrete IL-18, IL-12 p70 and IL-13 at this time pi, but produced higher amounts of IL-10 than C3H mice. Non of these cytokines was found increased in the cell supernatants of chronically infected mice. The addition of lipopolysaccharide (LPS) or Concanavalin A (Con A) to the cell cultures did not enhance the production of IL-18 and IL-12 at the time points tested. On the other hand, at 21 days pi, when parasitemia peaked, an inhibition of both the LPS induced IL-10 release and the IL-13 production upon Con A stimulation was observed in C3H, but not in BALB/c mice. We did not find an increase of IL-18, IL-10, or IL-12 p70 in the serum of the infected mice, despite the high seric IL-12 p40 concentrations reached during the infection. The data show that the different kinetics of the production of these cytokines in the spleen of both mouse strains could have a key role in the in vivo regulation of IFN-gamma production. In these experimental models, early IFN-gamma release and thus resistance to T. cruzi infection, could be related to the combined effect of both IL-18 and IL-12p70 in the absence of IL-13.

Acute Disease↗
PubMed2001

Partial protection and intrathecal invasion of CD8(+) T cells in acute canine distemper virus infection.

Initial non-inflammatory demyelination in canine distemper virus infection (CDV) develops against a background of severe immunosuppression and is therefore, thought to be virus-induced. However, recently we found a marked invasion of T cells throughout the central nervous system (CNS) in dogs with acute distemper despite drastic damage to the immune system. In the present study, this apparent paradox was further investigated by immunophenotyping of lymphocytes, following experimental CDV challenge in vaccinated and non-vaccinated dogs. In contrast to CDV infected, unprotected dogs, vaccinated dogs did not become immunosuppressed and exhibited a strong antiviral immune response following challenge with virulent CDV. In unprotected dogs rapid and drastic lymphopenia was initially due to depletion of T cells. In peripheral blood, CD4(+) T cells were more sensitive and depleted earlier and for a longer time than CD8(+) cells which recovered soon. In the cerebrospinal fluid (CSF) we could observe an increase in the T cell to B cell and CD8(+) to CD4(+) ratios. Thus, partial protection of the CD8(+) cell population could explain why part of the immune function in acute distemper is preserved. As found earlier, T cells invaded the CNS parenchyma in these dogs but also in the protected challenged dogs, which did not develop any CNS disease at all. Since markers of T cell activation were upregulated in both groups of animals, this phenomenon could in part be related to non-specific penetration of activated T cells through the blood brain barrier. However, in diseased animals much larger numbers of T cells were found in the CNS than in the protected dogs, suggesting that massive invasion of T cells in the brain requires CDV expression in the CNS.

Acute Disease↗