Ms OH C 40 years was addressed in MRI for headache associated with alertness disorder. Nocturnal insomnia and diurnal somnolence, left hemiparesis and extrapyramidal syndrome were noted and a slight fever. Brain CT showed diffuse hypodensity on the central gray nuclei without significant contrast enhancement. MRI was performed on a high-field device 1.5 T siemens in the 3 planes with T1 SE, T2 SE, T2 FLAIR, T2* and T1 gadolinium sequences.

The biological examinations showed a biological inflammatory syndrome with elevation of CRP without abnormality on the blood. Serum IgM testing by CATT showed positivity; the lumbar puncture detected trypanosomes in the CSF.

MRI showed predominant vasogenic cerebral edema on the gray nuclei and the right semi-oval center. Small focus of cytotoxic edema on the right internal capsule. Achievement of the thickened and hypersignal right optical strip. Minimal contrast. Discreet mass effect on the right lateral ventricle dispite the extending edema (Figures 1-3).

Meningo encephalitis stage of HAT.

The treatment was admistered in the trypanosomiasis specialized center and was based on pentamidine 200 mg/day intramuscular injection associated with arsobal 180 mg/day, dexamethasone 24 mg/day and ampicillin 4000 g/day. Administration of serum glucose 1.5 to 2 L/day with addition of NaCl, KCl and multivitamin complex.

Mr M K, 45 years old, chronic ethyl soil, was admitted to the emergency room for alteration of consciousness associated with a tremor. Fever was not noted. Abnormal somnolence has proceeded about a month. MRI scan was done using the same protocole.

They had shown an inflammatory syndrome with elevated CRP, a slight microcytosis without anemia and a slight neutrocytosis. Detection of serum IgM anti-trypanosomes by CATT and the search for trypanosomes on the CSF was positive.

The lumbar puncture showed hyperproteinorachia, hypoglycorachia and hyperchlorurorachia.

MRI showed bilateral vasogenic diffuse edema on the gray nuclei, semi-oval centers, protuberance and cerebral peduncle. Reaching of the right optical tract was noted. Little mass effect. No haemorrhage or significant contrast enhancement were noted (Figure 4 and Figure 5).

Encephalitic stage of HAT.

The same protocole was performed at the trypanosomiasis specialized center.

Natural history of HAT is classically divided into 3 phases. The inoculation stage induced by the bite of the tsetse fly causes a local inflammatory reaction called trypanoma. It leads to focal induration with erythema, local elevation of tem- perature and hyperaesthesia. After regression about 3 weeks, it leaves a hyperpigmented scar that can last several years.

The haemolymphatic stage is characterized by the importance of general signs with fever, lymphadenopathy, generalized pruritus, rash, edema, anemia, cardio- vascular and endocrine disorders, renal involvement and infections. Mainly, pulmonary infection can cause death.

The encephalic stage is characterized by disorders of alertness, sleep disorder with diurnal somnolence and night insomnia, leading to permanent hypersomnia and coma, which are the main characteristic of this HAT. This desease is also called “sleeping sickness”. Other abnormalities of the nervous system are also noted; motor and tonus disorders, modification of archaic osteo-tendinous and cutaneous reflexes, sensory disturbances with cutaneous and deep hyperaesthesia, psychiatric disorders, electrogenesis disorders [2] [4] [5] .

The parasite gets into the nervous system through the leptomeninge, reaching the sub-arachnoid space where it becomes detectable in the CSF. It finaly gets in the brain tissue through the Virchow-Robin spaces [6] . It induces a perivascular inflammatory reaction. If CT is normal at this stage, MRI may show meningeal or parenchymal abnormalities. In addition, MRI can differentiate between the lesion induced by the parasite and that due to melarsopol induced-encephalitis. Arsenical derivative forming part of the therapeutic arsenal of encephalitic form [2] [6] .

The HAT performs focal lesions, typically bilateral and quite symmetrical, on the grey nuclei, the cerebellum and the splenium of the corpus callosum [5] [6] . Later, diffuse hyperintensity is observed on the internal capsula, the external and extreme capsula associated with an attack of the cortex and deep grey nuclei. These aspects were noted in our two patients but without involvement of the cortex or the corpus callosum. The involvement of the optical pathways and the brainstem seems to be caracteristical (Figure 1 and Figure 2). In the case reported by Sabbah there was a meningeal or medium cerebellar peduncle lesion initially. There is no gadolinium enhancement. In our patients, signal of the lesions was predominantly a vasogenic edematous type; hyposignal T1, hypersignal T2, without zone of significant restriction. In the patient of the observation 1, the small restriction zone on the posterior arm of the internal capsula explained the partial deficit clinically described. It’s a singular remark that there was no focus haemorrhage.

Through our two observations and the cases reported in the literature, the typical aspects of HAT result in bilateral and quasi-symmetrical vasogenic edema involving the basal ganglia, the white matter, the brainstem. There is no significant contrast enhancement or mass effect despite the extending edema. Reaching of the visual pathway, the optic tract particularly seems characteristic in our 2 observations (Figure 2(a) and Figure 5(b)). We have not found in the rewiew of the litterature involvement of the optic tract in patient suffering from HAT. However in the case reported by Gill et al. involvement of the optic radiation have been discribed [6] [7] [8] .

These topographic and signal features of the HAT make possible to evoke the diagnosis before launching aetilogical research. MRI also make possible to distinguish lesions due to HAT from an arsenical encephalitis induced by melarsoprol administered during the treatment. It is a serious complication since it is fatal to 5% and whose survival is burdened with heavy sequelae. Checkley et al. reported a case of survival at the cost of a locked-in syndrome. Arsenical encephalitis typically results in haemorrhagic lesions with severe edema [5] [7] [9] .