Memory loss and pneumonitis - Europe PMC

CASE REPORT * ETUDE DE CAS

Memory loss and pneumonitis after anaphylaxis due to an insect sting Jorge A. Mazza,* MD, FRCPC; D. William Moote,* MD, FRCPC; J. Brian Gamble,t MD, CCFP; G. Bryan Young,4 MD, FRCPC A naphylaxis occurs suddenly and is the most memory loss, a dry, hacking cough and swelling of severe manifestation of an allergic reaction; the joints, and he complained that his eyes hurt, the symptoms include swelling, urticaria, especially when exposed to bright light. breathing difficulties, cardiovascular collapse and The patient presented to the Allergy Clinic, gastrointestinal discomfort.' We present a patient Victoria Hospital Corporation, London, Ont., about with an anaphylactic reaction in whom rare, long- 10 days after the initial episode. He looked determ changes developed. pressed but was otherwise healthy except for an enlarged spleen. A chest x-ray film showed pneumonitis. Although the findings at neurologic examinaCase report tion were normal he was thought to have a neurologA 38-year-old atopic man suffered a severe ic and not a psychologic problem because he deanaphylactic episode after being stung by an insect scribed an almost abulic state (absence of or inability he described as a "yellow jacket." Ten days earlier to exercise willpower) and complained of confusion, he had been stung twice without reaction. Within 2 disorientation and impaired memory. A neuropsychologic evaluation revealed impairminutes after being stung on the second occasion typical anaphylactic symptoms - swelling of the ment in the free recall of verbal material, delayed face and hands, breathing difficulties and light-head- recognition of nonsense figures and both an immediedness - developed. Although he did not lose ate and a delayed recognition of faces. Another chest consciousness he felt dizzy and had to lie down. A x-ray film showed pneumonitis of the lingular segwitness injected him immediately with 0.3 mL of ment of the left upper lobe. Laboratory investigaepinephrine (1:1000 solution) subcutaneously. With- tion, including urinalysis and tests for immune in 45 minutes he arrived at the community hospital complexes (Cl q binding assay), total complement (in and was found to be normotensive. He was given CH50 units), C3 and C4 levels, blood cell and two subcutaneous injections of epinephrine (at the differential counts, electrolyte levels and biochemissame dosage and concentration as the first) and try profile (SMA 12), gave normal results. The pneumonitis resolved spontaneously 10 diphenhydramine, 50 mg intramuscularly. He was days after presentation to the Allergy Clinic. discharged 2 days later. Magnetic resonance imaging of the brain perThe patient was readmitted after 3 days because of a sudden onset of excessive fatigue, confusion, formed 20 days after the initial episode gave normal headache, disorientation and an inability to concen- results. An electroencephalogram showed a nonspetrate or to initiate movement. He was thought to be cific abnormality in the temporal region on the left depressed. His blood chemistry was normal, and he side and similar changes on the right side, which was given lorazepam, 0.5 mg four times daily, and were compatible with the patient's difficulty in discharged. By this time there was evidence of some recognizing faces (prosopagnosia). From the departments of *Medicine, Ontario, London, Ont.

tNeurology and tFamily Medicine, Victoria Hospital Corporation and University of Western

Reprint requests to: Dr. Jorge A. Mazza, 208-111 Waterloo St., London, ON N6B 2M3 -

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Viral studies of a stored blood sample obtained 20 days after the sting, when the chest x-ray film still appeared abnormal, were done 1 year after the patient presented to the Allergy Clinic. The results were in the middle range of positive for herpes simplex types 1 and 2, varicella-zoster virus and

Mycoplasma. Almost 2 years after the initial episode the patient still had difficulty recognizing faces and had some impairment of verbal memory.

Comments

area.3 This single layer of cells is the most vulnerable to ischemic damage. Blythe and associates4 found that the IgE-mediated reaction in the lungs of rats challenged with antigen caused alveolar and interstitial edema and focal peribronchiolitis resembling pneumonitis. Although our patient's pneumonitis could have been a coincidental viral infection, the viral studies revealed results in the middle range of positive, not suggestive of a current infection. We unfortunately did not obtain a convalescent serum sample for confirmation. The enlarged spleen may have been due to an infection but was more likely a reaction to the serum sickness or a delayed allergic reaction. Although the clinical features of the case we have presented were typical of anaphylaxis the neurologic complications were not. They have not been reported in other large series of cases of anaphylaxis.',5 We could not prove that the symptoms were a direct result of the anaphylaxis or the ensuing serum sickness; however, they should be looked for after severe anaphylactic episodes.

The dramatic manifestations of anaphylaxis are usually triggered by an IgE-mediated release of potent biochemical mediators. Non-IgE-mediated reactions may involve the release of the same mediators and thus similar end-organ responses. These biochemical mediators are responsible for the anatomic findings, such as edema, cellular infiltrates and tissue damage, seen in fatal systemic anaphylaxis. In the lungs acute hyperinflation occurs, and secretions, submucosal edema, vascular congestion and eosinophilic infiltrates are present diffusely in References the bronchi. Tissue injury is the final step in serum sickness: tissue-damaging enzymes are released from 1. Sheffer AL: Anaphylaxis. J Allergy Clin Immunol 1985; 75: 227-233 the lysosomal system of neutrophils exposed to immune complexes. Wasserman SI: Mediators of immediate hypersensitivity. J We could find no previous case in the literature 2. Allergy Clin Immunol 1983; 72: 101-114 of anaphylaxis from an insect sting associated with memory loss or pneumonitis, or both. Nevertheless, 3. Zola-Morgan S, Squire L, Emeral B: Human amnesia and the we believe that our patient's memory loss and medio-temporal region. Enduring memory impairment following a bilateral lesion limited to field CAl of the hippocampus. pneumonitis were due to the release of biochemical JNeurosci 1986; 6: 2950-2967 mediators in his IgE-mediated allergic reaction.2 The memory loss was most likely due to ischemic necroBlythe S, England D, Esser B et al: IgE antibody mediated sis of the CAl area of the hippocampus caused by 4. inflammation of rat lung: histologic and bronchoalveolar the mediators. In a patient with memory loss (relavage assessment. Am Rev Respir Dis 1986; 134: 1246-1251 stricted memory and inability to record new memories) after a series of cardiac arrests a postmortem 5. Bacal E, Patterson R, Zeiss CR: Evaluation of severe (anaexamination showed selective damage of the same phylactic) reactions. Clin Allergy 1978; 8: 295-304

Allergy Some men also have strange antipathies in their natures against that sort offood which others love and live upon. I have read of one that could not endure to eat either bread or flesh; of another that fell into a swoonding fit at the smell of a rose.... There are some who, if a cat accidentally come into the room, though they neither see it, nor are told of it, will presently be in a sweat, and ready to die away. -

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Increase Mather (1639-1723)