Neurotrichinosis

Abstract

The clinical features, brain computerized tomography (CT) scans and cardiological findings of nine patients with neurotrichinosis are reviewed. Neurological signs consisted of encephalopathy and focal deficits with small hypodensities in the cortex and white matter, detected by the CT scans. Various cardiovascular events were also observed in eight out of nine patients. They were usually concomitant with neurological symptoms and mainly consisted of myocardial injury as assessed by electrocardiographic and plasma creatine phosphokinase (CPK)-MB isoenzyme changes. The cardio-neurological syndrome developed early in the course of the disease at a time of marked hypereosinophilia and the percentage of patients with eosinophilia > or = 4000 mm3 was significantly higher in the patients with neurological dysfunction than in those without neurological signs. We selected the following criteria to describe the distinctive cardio-neurological syndrome related to trichinosis: (i) early onset of neurological symptoms (within a few days) after the first general symptoms; (ii) central nervous system involvement consisting of both diffuse encephalopathy and focal neurological deficits, usually of simultaneous onset; (iii) concomitant acute myocardial injury and/or infarction; (iv) marked hypereosinophilia (> or = 4000/mm3) at time of first cardio-neurological events; (v) brain CT scan showing small hypodensities in the hemispheric white matter or cortex. Post-mortem examination of one patient revealed ischaemic lesions with multiple arteriolar microthrombi in the brain and myocardium. This was consistent with the brain CT scan and electrocardiographic data and suggested that neurotrichinosis is an expression of a multi-organ disorder associated with hypereosinophilia, that is characterized in most patients by simultaneous neurological and myocardial manifestations basically related to ischaemia.

Trichinosis

“…Brain lesions may involve both gray and white matter, cerebellum, pons and spinal cord. (16,29,35,46,56,67).…”

Severe trichinellosis with neurological involvement - neurotrichinellosis: A case report

“…The number of eosinophils in our patient at admission was 5,400/mm 3 , which corresponds to hypereosinophilia. According to Fourestie et al(1993), patients with eosinophilia higher than 4,000/mm 3 during trichinellosis are more likely to develop neurologic dysfunction than to not exhibit neurologic signs, and the level of eosinophilia correlates with the intensity of infection (Fourestie et al 1993).…”

Electrocardiographic changes and myocarditis in trichinellosis: a retrospective study of 154 patients

“…Compton et al (1993) reported a case of trichinellosis who required a pacemaker to maintain a normal cardiac rhythm, after developing respiratory failure, myocarditis and sinus arrest; a year after treatment with benzimidazole and corticosteroid, this patient appeared healthy (although still fitted with a pacemaker). Fourestie et al (1993) reported cardiovascular events in eight of nine patients with neurotrichinellosis, and suggested that hyper-eosinophilia was possibly implicated in the genesis of the cerebral and cardiac lesions seen during trichinellosis. Although the exact causes of the cerebral and cardiac abnormalities seen in some patients with neurotrichinellosis remain unknown, several pathogenetic mechanisms have been proposed (Ryczak et al, 1987).…”

“…Severe forms are characterized by visceral complications involving various organs, especially the lungs, heart and central nervous system, sometimes with a fatal outcome (Evdokimov, 1983). In neurotrichinellosis, cardiac involvement may occur early in the course of the disease, concomitant with the neurological symptoms (Fourestie et al, 1993). Most cardiac involvement in human trichinellosis is asymptomatic and only detected, if at all, during routine electrocardiographic (ECG) examinations.…”