[Miliary tuberculosis]. / La miliaire tuberculeuse,une série rétrospective marocaine.

INTRODUCTION: Tuberculosis miliary is a severe and rare form of tuberculosis. It is often due to a haematogenous spread of the bacillus of Koch and represents less than 2 % of tuberculosis. PATIENTS AND METHODS: We conducted a retrospective study of 81 cases of tuberculous miliary collected at the Department of respiratory diseases of the Ibn Rochd university hospital in Casablanca between September 2003 and November 2016. RESULTS: A female predominance was noted with 58 % of the cases. The average age was 36 years. The history of tuberculosis was found in eight cases and tuberculous tuberculosis in eleven cases, postpartum in five cases, diabetes in three cases and trisomy 21 in one case. The clinical picture was dominated by altered general status in all cases, and fever in 69 cases (86 %). Chest x-ray showed a miliary aspect in all cases, cardiomegaly in two cases, pyopneumothorax in three cases, and opacities excavated in five other cases. The intradermal tuberculin reaction, performed in all cases, was positive in 26 cases, and sputum oscillations were positive in 21 cases. The dissemination report found cerebromeningeal involvement in nine cases, with cerebral tuberculomas in five cases, pericarditis in four cases, mediastinal and peripheral adenopathies in nine cases each. Bouchut tubercles were found in nine cases. Antibacillary therapy was started as a matter of urgency, according to the national TB control program with the old regimen (2SHRZ/7RH) and the new regimen (2RHZEb/7RH) in all cases. The outcome was good in 55 cases (68.9 %), 17 patients were lost to follow-up, and 11 deaths were reported. CONCLUSION: We insist on this work on the severity of the tuberculous miliary and the need for early and urgent therapeutic management.

The normal distribution of PRNP codon 129 polymorphism in the Moroccan population (Arabs and Casablanca residents).

The common prion protein gene (PRNP) codon 129 polymorphism is a strong susceptibility factor for human prion diseases. In this study, we examined the allelic variation of methionine and valine at codon 129 in 147 subjects representing the normal Moroccan population. The sharing of the genotype was 57.1% for Methionine-Methionine (MM), 36% for Methionine-Valine (MV), and 6, 8% for Valine-Valine (VV). These results are indeed intermediate between those discovered at the European and Asian populations. However, and for a better assessment of the risk to develop prion diseases in the Moroccan population, the survey of the frequency of the codon 219 polymorphism is required.

Alpha-synuclein accumulates in the brain of scrapie-affected sheep and goats.

Immunohistochemical examination demonstrated widespread granular deposits of alpha-synuclein (alphaSN) in the brains of sheep and goats with natural scrapie, especially in the cornu ammonis and subiculum of the hippocampus; this contrasted with the diffuse and non-granular immunolabelling seen in healthy controls. There was non-regular "co-localization" of PrP(Sc) and alphaSN. The findings resembled those reported in Creutzfeldt-Jakob disease and in experimental prion disease in hamsters and mice. The results suggest that perturbation of alphaSN metabolism plays a role in human and animal prion diseases.

[Snake bite poisoning and compartment syndrome. A report of two cases]. / Envenimations par morsure de serpents et syndrome de loge. A propos de deux observations.

Snakebite poisonings are frequent In Morocco, because of the delay in treatment, they can be very serious even lethal. Treatment has two components: firstly correction of the systemic hemodynamic, respiratory and haematological disturbances and secondly administration of specific antivenom. Envenomation of a limb can lead to cutaneous necrosis, compartment syndrome and even necrotising fascitis. Early diagnosis and prompt treatment is needed to prevent these complications. We report two cases of compartment syndrome of which one was combined with systemic manifestations and the other caused residual pathology in the limb.

[Familial fronto-temporal dementia with brain stem ubiquitin-positive neuronal inclusions]. / Démence fronto-temporale familiale avec inclusions marquées par l'anti-ubiquitine dans le tronc cérébral.

INTRODUCTION: Fronto-temporal dementias (FTD) were described a century ago on the macroscopic basis of frontal and/or temporal lobe atrophy. Progress in neuropathology, immunohistochemistry, biochemistry and genetics has since shown that they are heterogeneous entities, encompassing many different diseases with similar clinical presentations. A few, such as tauopathies due to mutations of the gene coding for tau protein (MAPtau form a well-defined group. Definition and grouping of other types of FTD is still problematic. MATERIAL AND METHOD: We studied a family where the mother and 4/8 children were affected with FTD. Clinical presentation was typical of FTD. Onset was ill-defined with early (at age 40 years or less) personality changes. The clinical course was protracted (about 30 years). For a long period, the patients were able to live in the community in spite of obvious signs such as hyperorality and loss of verbal initiative; operative orientation as to place was preserved for a long time: a mute patient was still able to drive. Signs of extrapyramidal or motoneuron involvement were not observed. RESULTS: The genetic study failed to detect any mutation in MAPtau; the lod score for flanking markers was positive but not significant. Biochemical study showed no qualitative abnormality in tau protein. Neuropathological study of one affected subject showed brain atrophy (962 g), with elective frontal lobe involvement. Cortical nerve cell loss was more marked in superficial layers and in frontal areas; glia was inconspicuous; pseudolaminar spongiosis was present in the more severely affected zones. No argentophilic "Pick bodies" were seen; ubiquitin-positive, tau-negative round inclusions were present in the cytoplasm of fascia dentata neurones. "Tangles" were mostly restricted to the entorhinal cortex, partly correlated with tau immunoreactivity, but better with ubiquitin immunoreactivity. Large, ovoid or reniform, moderately dense, spongy, granular or filamentous argentophilic cytoplasmic nerve cell inclusions were observed. They were ubiquitin-positive, but did not react with other antibodies, particularly anti-tau. They were present in swollen nerve cells in the deeper cortical layers but were most conspicuous in the brain stem: in the magnocellular reticular nuclei (e.g. nucleus centralis pontis), in the pes pontis, in the inferior olive and in motor nuclei, especially in the trigeminal motor nucleus. They were not associated with nerve cell loss, atrophy nor pycnosis. Cerebellar relay nuclei neurones were swollen, and their cytoplasm contained argentophilic filaments. CONCLUSION: In our opinion, "ubiquitinopathy" would be non-specific and "Motor Neuron Disease-Inclusion Dementia" (MNDID) would not be satisfactory as a diagnosis for the present cases of FTD. Hopefully, progress in genetics may allow a causal, and thence definitive, classification.

Ultrastructural localization of parkin in the rat brainstem, thalamus and basal ganglia.

The parkin gene encodes a 52 kd putative E3 ubiquitin-protein ligase involved in an autosomal recessive form of early onset parkinsonism. Parkin ultrastructural localization was studied by immunohistochemistry in the adult rat brain and in a parkin inducible PC12 cell line (HS22). In the rat brain, parkin immunoreactivity was detected in neuronal and glial cell bodies and in nerve processes. In the neurons, it was mostly localized on the periphery of large vesicles, some rare mitochondria and endoplasmic reticulum in the cell bodies, and on the periphery of large vesicles in the dendrites and terminals of the neurons. In addition, parkin immunoreactivity was also found around synaptic vesicles in the presynaptic elements of some axons. In HS22 cells over-expressing parkin, the distribution of the protein was similar to that observed in the perikarya of the labeled neurons.

[Surgical treatment of capitellum fractures in the adult. Eight case reports]. / Traitement chirurgical des fractures du capitellum chez l'adulte. A propos de huit cas.

Fracture of the capitellum is a rare intra-articular fracture and presents a frontal fracture line. It occurs in adolescents after the age of 13 years and in adults. We report a series of eight patients treated between 1992 and 2002. There were five females and three males with a mean age of 25 years (range: 20-34 years). According to the classification of Bryan and Morrey, three fractures were classified as type I, three as type II and two as type III. All patients were operated on within the first week after injury. The fixation techniques used were screw fixation in five cases and Kirschner wire fixation in three cases. Seven patients had excellent results and one patient had some limitation of range of movement. There were no instances of infection or avascular necrosis. Diagnosis of this fracture is often missed. Poor results of treatment are observed after imperfect reduction, delayed treatment or resection of the capitellum. We report in this study the results of surgical treatment.

[Giant cell tumor of the third metacarpal bone: a case report]. / Tumeur à cellules géantes du troisième métacarpien: à propos d'un cas.

A case of giant-cell tumor of the third metacarpal bone is reported, treated with resection and reconstruction by iliac graft. At a 5 years follow-up, the cosmetic and functional results of the hand are good.

[Tuberculous infection after dynamic-hip screw osteosynthesis: a case report]. / Infection tuberculeuse de hanche après ostéosynthèse par vis plaque: à propos d'un cas.

We report the case of a 72-year-old woman who developed osteoarticular tuberculosis after dynamic hip screw osteosynthesis for a pertrocanteric fracture. Necrosis of the head and disassembly of the prosthetic material ensued. This patient had no history of pulmonary or extra-pulmonary tuberculosis. Certain diagnosis was established on the basis of pathology findings and successful antibiotic treatment associated with surgery: ablation of the implant, head-neck resection, total hip arthroplasty. Two hypothetical pathogenic mechanisms can be put forward: hematogenic dissemination from another focus and reactivation of latent local infection.

[Complete brachial plexus paralysis in anterior shoulder dislocation: a case report]. / Paralysie complète du plexus brachial au cours d'une luxation antéromédiale de l'épaule: à propos d'un cas.

Brachial plexus paralysis secondary to anterior dislocation of the shoulder is a rare injury. The authors report a case of traumatic anterior dislocation of the shoulder complicated by brachial plexus palsy. Recovery took a whole year and the patient was left with residual shoulder stiffness.