NEUROL-2380; No. of Pages 7 revue neurologique xxx (2020) xxx–xxx Available online at ScienceDirect www.sciencedirect.com Brief Report 3 Tesla serial magnetic resonance imaging of human African trypanosomiasis (Trypanosoma brucei gambiense) and review of the literature M. Boukobza a,*, S. Lariven b, S. Houze c, J.-P. Laissy a,d,e a Department of Radiology, Bichat University Hospital, AP–HP, 75018 Paris, France Infectious and Tropical Diseases Department, Bichat-Claude Bernard University Hospital, AP–HP, 75018 Paris, France c Parasitology and Mycology Laboratory, Bichat-Claude Bernard University Hospital, AP–HP, 75018 Paris, France d Inserm U1148, Paris, France e Bichat Hospital, University Paris, Paris, France b info article abstract Article history: We report serial magnetic resonance imaging (MRI) findings and follow-up in a case of Received 21 April 2020 human African trypanosomiasis (HAT) presenting with limited lesions followed by early and Received in revised form complete resolution. We searched the literature for documented cases and reviewed MRI 26 July 2020 findings before treatment. A 30-year-old Lebanese man, who had lived in Gabon for six Accepted 10 November 2020 years, presented with a two-year history of rash, anorexia, weight loss, arthralgia, pares- Available online xxx thesia, and hypersomnia. Previously, the patient had received corticosteroid therapy for Keywords: on the left arm located at the site of an old insect bite, enlarged cervical, axillar and inguinal Trypanosoma brucei gambiense lymph nodes, hepatosplenomegaly and impaired concentration. Blood analysis showed an unconfirmed ANCA-associated vasculitis. Physical examination revealed a painless chancre Sleeping sickness elevated protein level (90 g/L) with hypoalbuminemia (24.2 g/L) and elevated IgM (26.4 g/L). MRI Bone marrow aspirate and biopsy failed to detect any parasite. Polymerase chain reaction Hypothalamus tests on blood and cerebrospinal fluid were positive for Trypanosoma. Serology tests confir- Human African trypanosomiasis med the diagnosis of HAT due to Trypanosoma brucei gambiense infection. 3T MRI showed Encephalitis lesions in the hypothalamus and basal ganglia, the internal capsule, and the mesencephalon bilaterally. Follow-up MRI showed interval progression of the abnormalities. Treatment with melarsoprol was followed by clinical improvement with regression of the lesions on the three-month MRI, then total resolution at the 10-month follow-up. This case highlights a pattern of mild MRI lesions in T. brucei gambiense HAT with a total and rapid resolution under treatment. The literature review (16 HAT cases with sufficient radiological data, included ours) revealed an MRI pattern of brain lesion distribution that could be helpful for diagnosis and orienting biological tests. # 2021 Elsevier Masson SAS. All rights reserved. * Corresponding author. E-mail addresses: m.boukobza@orange.fr (M. Boukobza), sylvie.lariven@aphp.fr (S. Lariven), sandrine.houze@aphp.fr (S. Houze), jean-pierre.laissy@aphp.fr (J.-P. Laissy). https://doi.org/10.1016/j.neurol.2020.11.002 0035-3787/# 2021 Elsevier Masson SAS. All rights reserved. Please cite this article in press as: Boukobza M, et al. 3 Tesla serial magnetic resonance imaging of human African trypanosomiasis (Trypanosoma brucei gambiense) and review of the literature. Revue neurologique (2021), https://doi.org/10.1016/j.neurol.2020.11.002 NEUROL-2380; No. of Pages 7 2 revue neurologique xxx (2020) xxx–xxx 1. Introduction We report 3 Tesla serial magnetic resonance imaging (MRI) findings in a patient with human African trypanosomiasis (HAT) due to Trypanosoma brucei gambiense infection. Complete clinical recovery, achieved at 10-month follow-up, was associated with total involution of all MRI-detected lesions. We describe a specific pattern of basic MRI abnormalities observed in our patient and in earlier reported cases with imaging follow-up. 2. Case report A 30-year-old Lebanese man who had lived in Gabon for six years, sought care for an insect bite on his left arm. Physical examination disclosed local rash with edema and pruritus at the site of the old insect bite, fever, anorexia, weakness, weight loss, headaches, arthralgia, paresthesia of the lower limbs, and hypersomnia. The patient reported an earlier hospitalization in Lebanon where ANCA-related vasculitis had been suggested as a possible diagnosis but without confirmation. He had received corticosteroid therapy as treatment. His hypersomnia had worsened prior to the current consultation. The patient was admitted to our hospital two years after his first manifestations. Physical examination confirmed the presence of a painless chancre on the left arm at the site of an old insect bite and local rash. Enlarged cervical, axillar and inguinal lymph nodes were noted, as well as hepatosplenomegaly. The neurology examination was normal except for the presence of impaired concentration. Three days after the initial in-hospital examination, the patient had a generalized tonic-clonic seizure and was given levetiracetam (200 mg/kg). Blood analysis showed an elevated protein level (90 g/L) with hypoalbuminemia (24.2 g/L) and elevated IgM (26.4 g/L), without monoclonal immunoglobulin. Cerebrospinal fluid (CSF) studies showed a white blood cell (WBC) count at 39/ mm3 (100% lymphocytes), protein at 0.82 g/L with a normal CSF/serum glucose ratio. CSF bacterial, fungal and viral cultures were negative. EEG was suggestive of encephalopathy. Thoracic and abdominopelvic computed tomography showed thoracic and sub-diaphragmatic lymphadenopathies that were hypermetabolic on 18F-FDG positron emission tomography. The diagnosis of HAT was considered. Bone marrow aspirate and biopsy as well as inguinal lymph node biopsy failed to detect any parasite. Blood and CSF polymerase chain reaction (PCR) tests were positive for Trypanosoma and serology was positive for T. brucei gambiense in both serum and CSF (indirect immunofluorescence 1/200 and 1/50, respectively). Brain MRI fluid-attenuated inversion recovery (FLAIR) sequence showed abnormal hyperintense signal in the basal ganglia (caudate nuclei, putamen), thalami, internal capsule, hypothalamus, pons and ventral mesencephalon (Fig. 1a–f). All the lesions exhibited a bilateral and almost symmetric distribution. There were no abnormalities on diffusionweighted imaging (DWI) and T2* sequences; there was no enhancement. The treatment regimen consisted in a seven- day course of nifurtimox-eflornithine combination therapy, associated with levetiracetam. A follow-up MRI performed at eight days showed an interval improvement in the FLAIR hypersignal in all the lesions (Fig. 1g and h). Repeat CSF analysis on the same day showed WBC 3/mm3 and protein 1.10 g/L; follow-up serum serology remained positive for T. brucei gambiense. A twomonth MRI showed only a minimally FLAIR hypersignal at the ventral mesencephalon, the internal capsule and the internal part of the globus pallidus bilaterally. The FLAIR hypersignal of the caudate nuclei, thalami and hypothalamus had disappeared (Fig. 1i). The 10-month MRI showed complete resolution of the lesions and mild supratentorial atrophy, compared to the admission MRI. After treatment, the CSF analysis normalized. In parallel, six weeks after treatment initiation, clinical symptoms progressively resolved, with a decrease of the skin rash, weakness, headaches, arthralgia and hypersomnia. Only minor concentration disorders remained at the time of this report. 3. Discussion Two important aspects of the diagnosis of HAT must be considered: neuroradiological and biological. Our case presents MRI particularities, compared to the literature cases. First, the MRI lesions were relatively limited and their clinical-radiological regression was rapid, despite corticosteroid therapy, which could have aggravated the situation. Furthermore, corticosteroid therapy could have masked the symptoms and confounded the diagnosis, which may explain the delay in diagnosis. Second, the presence of a hypothalamus hypersignal on FLAIR sequence, which improved and resolved concomitantly with the other MRI lesions, is unusual. The presence of a high IgM level, both in blood and CSF, is helpful to establish the diagnosis of HAT at an early stage [1]. According to WHO criteria, a WBC count > 5 cells/mL is considered indicative of central nervous system involvement [2], although other authors have suggested a cut-off of > 20 cells/mL [3,4]. In our case, the 39 WBCs in the CSF, along with the elevated IgM level, are in favor of the diagnosis of HAT. Reports on MRI features of T. brucei gambiense HAT are scarce, because MRI equipment is not available in large numbers in endemic countries. The number of reported cases with MRI correlations has been increasing in developed countries over the past years (1996–2009: 6 cases; 2009–2019: 10 cases), but still remains limited compared with clinical and biological studies [1,5–15] (Table 1). MRI brain lesions are commonly reported as non-specific. However, based on the 16 reported cases, including ours, with enough MRI data obtained before treatment initiation [1,5–15], we observed that the lesions were in all cases bilateral and symmetric or almost symmetric, except for median structures, i.e. corpus callosum and hypothalamus (Table 1). We tried to describe the preferential sites and association trends, the MRI features of the lesions and to identify the most usual MRI patterns. Please cite this article in press as: Boukobza M, et al. 3 Tesla serial magnetic resonance imaging of human African trypanosomiasis (Trypanosoma brucei gambiense) and review of the literature. Revue neurologique (2021), https://doi.org/10.1016/j.neurol.2020.11.002 NEUROL-2380; No. of Pages 7 revue neurologique xxx (2020) xxx–xxx 3 Fig. 1 – Brain MRI before and after treatment: a–f: at admission. Fluid-attenuated inversion recovery (FLAIR) MRI sequence: hyperintensity in both lenticular nuclei, caudate nuclei, thalami and internal capsule (a and b), pons and ventral mesencephalon (c and d). Hypersignal is well identified on coronal T2 image at the internal capsules (e) and at the thalami and hypothalamus (f); g and h: follow-up MRI at 8 days post-treatment. One week after melarsoprol was initiated, MRI Please cite this article in press as: Boukobza M, et al. 3 Tesla serial magnetic resonance imaging of human African trypanosomiasis (Trypanosoma brucei gambiense) and review of the literature. Revue neurologique (2021), https://doi.org/10.1016/j.neurol.2020.11.002 NEUROL-2380; No. of Pages 7 4 revue neurologique xxx (2020) xxx–xxx First, basal ganglia and supratentorial white matter were the most frequently involved localizations (81.2% for both) with a bilateral distribution. Surprisingly, reviews on basal ganglia and/or thalamic lesions (bilateral or not) do not mention HAT [16–19]. Second, there were association trends. Bilateral supratentorial white matter lesions and bilateral basal ganglia lesions were frequently associated (68.7%). The following structures were very frequently involved: lenticular nuclei (81%); thalamus (56%); internal capsule (56%). The posterior fossa was involved in 75% of cases. Other associations must be highlighted, as they may be helpful for diagnosis. They include simultaneous involvement of the basal ganglia, thalami and brain stem seen in nine out of 16 cases (56.3%) and involvement of the basal ganglia, brain stem and supratentorial white matter also seen in nine out of 16 cases (56.3%); in addition, 11 out of 16 cases (68.7%) had internal capsule involvement. MRI lesions in patients with HAT have three main features. They are not associated with hemorrhages. But micro-hemorrhages have been reported in HAT after treatment [11 (cases 1,2,3)]. There is no apparent diffusion coefficient (ADC) restriction of the lesions. Patel et al. [11] found limited areas of restricted ADC in post-treatment MRI studies of lesions which included micro-hemorrhages that can introduce potential error in ADC evaluation. Post-contrast lesion enhancement has not been reported, except for one case with mild contrast enhancement of the basal ganglia reported by Gil et al. [9]; however, meningeal enhancement can occur [6,10]. Careful assessment of lesions outside the basal ganglia, such as involvement of the cortex, thalamus, or brain stem, may be helpful for differential diagnosis for patients who have lived in endemic regions. Other entities have preferential sites or specific imaging features, and the association or not of lesions in other sites must be considered for the differential diagnosis (Fig. 1j): i) bilateral thalami involvement is not associated with basal ganglia lesions in hypoglycemia [18], artery of Percheron infarction (which may extend to the mesencephalon), and top of the basilar artery syndrome (associated with ischemia of the posterior circulation territory); ii) specific locations are observed such as globi pallidi in carbon monoxide, ecstasy and intravenous heroin intoxication, or putamina in methanol intoxication; iii) cortical involvement – seen in encephalitis (flavivirus infections and Creutzfeldt–Jakob disease), hypoxicischemic encephalopathy, hypoglycemia, and ischemic entities mentioned above (top of the basilar artery syndrome and artery of Percheron infarction)–narrows the differential diagnosis. In addition, the presence of CSF lymphocytic pleocytosis points the diagnosis to encephalitis. Irrespective of lesion distribution and association, the presence of restricted diffusion – observed in hypoxia, hypoglycemia, ischemia, or carbon monoxide intoxication, but not a classic feature of HAT – should help narrow diagnostic considerations. The presence of massive hemorrhages – in the putamen or the basal ganglia, or of micro- or macro-hemorrhages in the thalami, along with marked hypointensity of the deep cerebral venous system, thrombus on T2* sequences, and concomitant variable alterations on DWI – help in the imaging diagnosis of methanol intoxication, cocaine intoxication and deep cerebral venous thrombus with parenchymal hemorrhage, respectively [20]. Contrast enhancement, which may be seen in case of infarction or encephalitis, is inconsistent in several entities and cannot orient the diagnosis. In addition, geographical origin (flavivirus encephalitis, Africa for HAT) and clinical presentation (acute onset for ischemia, hypoglycemia and intoxication, rapidly progressive onset for deep venous thrombosis, flavivirus encephalitis and Creutzfeldt–Jakob disease) are important tools for narrowing the differential diagnosis. Furthermore, the clinical context, especially for intoxication, hypoxia and hypoglycemia, is crucial. 4. Outcome The literature provides data on outcome with a perspective of at least one year in 14 cases (Table 1). Depending on the clinical course, three clinical-radiological patterns can be described, with an almost equal distribution: i) complete resolution (5/14; 35.7%) [1,7, 15, present case]; ii) clinical resolution with residual hyperintensities and mild atrophy (4/14; 28.6%) [8,9, 14 (case 3)]; iii) neurological sequelae with residual hyperintensities and mild atrophy (5/14; 35.7%) [3,6, 13 (cases 1 and 2)]. Neurological sequelae are dominated by mild memory disorders [3] and dysarthria [1]. In the only reported case of HAT in an infant, severe neurological sequelae were observed [13 (case 2)]. It should be noted that in Karger’s case [6], partial regression was noted at one-year follow-up, and at four years only remnants were observed. The literature review and the current case also show that early regression, even partial, is possible one or two months after treatment onset [12]. 5. Conclusion The reported case shows that HAT may be associated with minimal MRI lesions and early and total clinical-radiological regression. In most cases, MRI lesions consist in bilateral and symmetric or almost symmetric FLAIR and DWI hyperintensities of the basal ganglia and supratentorial white matter. examination shows a residual T2 hyperintensity in the thalami, hypothalamus (g) and internal capsules (h); i: follow-up MRI at 2 months post-treatment. Fluid-attenuated inversion recovery (FLAIR) MRI sequence shows a very residual hyperintensity in the internal capsules bilaterally; j: differential diagnosis of the diseases with bilateral basal ganglia, and/ or thalami, and eventually deep white matter involvement based on their magnetic resonance signal characteristics and on their apparent diffusion coefficient restriction values. HAT: Human African Trypanosomiasis BG: basal ganglia; CJD: Creutzfeldt-Jakob disease; Thal: thalami; BA: basilar artery; Percheron: Percheron artery infarct; FlaviV: Flaviviruses; DCVT: deep cerebral venous thrombosis; WM: white matter; CO: CO intoxication. Please cite this article in press as: Boukobza M, et al. 3 Tesla serial magnetic resonance imaging of human African trypanosomiasis (Trypanosoma brucei gambiense) and review of the literature. Revue neurologique (2021), https://doi.org/10.1016/j.neurol.2020.11.002 NEUROL-2380; No. of Pages 7 Cerebellar Author/ reference/ year 1 2 3 4 5 6 7 W Serrano– M Gonzalez, 1996 [5] E Sabbah, 30/M 1997 [6] W Bedat–Millet, 39/M 2000 [7] Clinical S-Tent CC LN CN Tha hTha IC WM EC Hippoc Midbrain Pons MO MCP WM Delay Clinical Sleepiness, 1 psychiatric disorders 0 1 0 0 0 0 0 0 1 0 0 0 0 0 1 0 0 0 0 1 0 0 0 0 0 1 0 0 0 1 0 0 0 0 0 0 1 0 0 0 0 0 1 0 1 0 0 1 0 1 0 0 0 MRI Resolution Resolution 1Y Dysarthria HS MCP 0 1Y Residual intellectual disturbances HS WM Sus-T 0 0 1Y Resolution Residual HS. Atrophy Residual HS. BS-atrophy Residual HS. BS Atrophy Resolution W Sahlas, 2002 [8] W Gill, 2003 [9] 42/M Fever, dynamic 0 cerebellar syndrome Sleepiness, 1 psychiatric, extrapyramidal syndrome Psychotic disorder 1 42/M Fatigue, somnolence 1 0 1 1 1 0 1 1 0 1 0 0 0 0 0 1Y Resolution W Kager, 2009 [10] W Elliott, 2014 [11] 27/F Apathy, sleepiness, 1 0 1 0 1 0 0 0 0 1 0 0 0 0 0 4Y Resolution 1 0 1 0 1 0 0 0 0 0 1 0 0 0 0 1.5 Y Resolution 1 0 1 0 1 0 1 1 0 0 0 0 0 0 0 2Y Slight memory disturbances Resolution 1 0 1 1 0 0 0 0 0 0 1 0 0 1 0 4m Resolution Resolution 1 0 1 0 1 0 1 1 0 0 1 0 1 1 0 1Y Not available Atrophy 1 0 1 0 1 0 1 0 0 0 0 0 0 0 0 6m Hypotonia – psychomotr disturbances Partial regression. Atrophy 1 1 1 1 0 0 1 1 0 0 0 0 0 0 0 4m Unsteadiness. Poor coordination Mild Sus-T atrophy 1 0 0 0 0 0 0 0 1 0 1 0 0 1 0 3m Improvement: mobility, cognition HS hippocamp 8 W Wengert, 2014 [1] 9 W Denny, 2016 [12] 10 W Gaillot, 2017 – Case 1 [13] W Gaillot, 2017 – Case 2 [13] 11 Age/ sex Follow-up 12 W Patel, 2018 – Case 1 [14] 13 W Patel, 2018 – Case 2 [14] 67/M Drowsiness, confusion, memory impairment 33/M Apathetic FL syndrome, sleep pattern 36/M Somnolence, ataxic gait, impaired concentration 22/F Ideomotor impairment, general hypotonia 13 m/M Psycho-motor retardation, axial hypotonia, dystonic movements (face, limbs) 58/M Fever, confusion, drowsiness, tremors, unsteadiness, poor coordination 62/M Personality change, somnolence, shuffling gait. lateral gaze palsy, rigidity, bradykinesia revue neurologique xxx (2020) xxx–xxx Please cite this article in press as: Boukobza M, et al. 3 Tesla serial magnetic resonance imaging of human African trypanosomiasis (Trypanosoma brucei gambiense) and review of the literature. Revue neurologique (2021), https://doi.org/10.1016/j.neurol.2020.11.002 Table 1 – Neurological signs and symptoms, Brain MRI findings and outcome in human African trypanosomiasis: 16 patients reported with enough radiological data. 5 NEUROL-2380; No. of Pages 7 6 Prevalence of lesions (%) 30/M W Present case, 2020 16 56/M W Boukobza, 2019 [15] 15 E: east Trypanosomiasis; W: west Trypanosomiasis; age in years; M: male; F: female; m: month; S-Tent WM: supratentorial white matter; CC: corpus callosum; LN: lenticular nuclei; CN: caudate nuclei; Thal: thalami; hThal: hypothalamus; IC: internal capsule; EC: external capsule; Hippoc: hippocampus; MO: medulla oblongata; MCP: middle cerebellar peduncle; DN: dentate nuclei; Y: year; BS: brain stem; HS: T2/FLAIR hypersignal. 6.25 6.25 12.5 18.7 81.2 31.2 56.3 12.5 56.3 37.5 6.25 43.7 37.5 25 Resolution Resolution 10 m 0 0 0 0 1 1 1 1 1 0 0 1 1 0 Resolution Resolution 1Y 0 1 1 1 1 1 1 0 1 1 1 1 1 0 HS residual WM Sus-T. Mild atrophy Hypotonia – psychomotor disturbances 6m 0 0 0 0 0 1 0 0 0 0 1 Fatigue, fever, 1 headache, somnolence, vertigo, diplopia. Sleepiness, impaired 0 concentration, ataxic gait Sleepiness, fatigue, 0 impaired concentration 81.2 38/M Patel, 2018 – Case 3 [14] E 14 Hippoc Midbrain Pons MO MCP WM Author/ reference/ year Table 1 (Continued ) Age/ sex Clinical S-Tent CC LN CN Tha hTha IC WM EC Cerebellar 0 0 0 Delay Clinical Follow-up MRI revue neurologique xxx (2020) xxx–xxx MRI is crucial in narrowing the differential diagnosis as it rules out entities that have a similar distribution of lesions: the presence of ADC restriction eliminates the diagnosis of HAT and cortical lesions are uncommon. Hence, MRI can help to orient appropriate biological tests. Funding This research did not receive any specific grant from funding agencies in the public, commercial, or not-for-profit sectors. 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