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Query: UMLS:C0018681 (headache)
 56,091 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

300 patients with sleeping sickness have been admitted, at the AHT clinic of Daloa, over a time period of 22 months. The sex ratio of the patients is 1.5 males for 1 female; the mean age is 25.5 years. The most frequent signs and symptoms observed by clinical examination are: fever (30%), nodes (86.3%), prurigo (43.3%), splenomegaly (15.3%), hepatomegaly (1%), headache (72.6%), vigilance and sleeping disturbances (68.7%), perioral reflexes (67.6%), cheiro-oral reflexes (64.3%), movement disorders consisting of tremor, choreo-athetosis movements, buccal dyskinesia or seizures (35%), motor palsy and gait disorders (15%), tonus disturbances (12.3%), sensitivity abnormalities (17%), endocrine disorders (16.3%), psychiatric symptoms (6.3%). According to CSF status, 261 patients have been classified in second period (P2). This group, although biologically well defined, is in fact a miscellaneous group of clinical signs and symptoms ranging from apparently normal patients to sleeping comatose and cachectic patients. 93% of the patients in this group have peripheral signs associated with neurological symptoms. They are as frequent in the first period as in the second period, with a statistical significance. This is an argument to think that the CNS is early affected in the course of the disease. The classification of the patients in groups of increasing neurological impairments, is in accordance with this hypothesis. 89% of the patients in the second period have only slight neurological signs. This explain how difficult it is for a physician to use melarsoprol in the treatment of all patients classified in second period.
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PMID:[The different present-day clinical picture of human African trypanosomiasis caused by T. b. gambiense. Analysis of 300 cases from a focus in Daloa, Ivory Coast]. 284 37

An American citizen acquired African trypanosomiasis while on a hunting safari in Sudan, East Africa. His travel history and rapid onset of symptoms, including fever, chills, headache, lethargy, and weight loss, were suggestive of Trypanosoma brucei rhodesiense infection, and trypanosomes were demonstrated in routine blood smears and buffy-coat preparations. Despite the presence of headaches, nuchal rigidity, and CSF pleocytosis, he was treated for non-CNS African trypanosomiasis, based on a normal CSF IgM level. This case report, along with a review of previously reported cases of imported African trypanosomiasis, illustrates the importance of clinical consideration of this rare, but often misdiagnosed, tropical illness in febrile patients returning from Africa.
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PMID:African trypanosomiasis in an American hunter in East Africa. 667 14

A case-control study was carried out in the Congo to define a scoring system based on a number of clinical and epidemiological criteria of African trypanosomiasis due to Trypanosoma brucei gambiense which could be used by peripheral health services to establish a diagnosis. The survey comprised 163 cases and 326 controls. Clinical signs and symptoms were fever, headache, pruritus and skin lesions due to scratching, diarrhoea, oedema, cervical adenopathies, sleep rhythm disturbances, changes in appetite, amenorrhoea or impotence, mental confusion, neurological signs, and other minor clinical disturbances. Other criteria were a history of previous trypanosomiasis and the presence of domestic animals in the home environment. Analysis of the results showed that neither a single criterion nor a group of criteria is pathognomonic for the disease. The selected criteria do not allow discrimination of sleeping sickness patients among suspected individuals who present themselves. A scoring system is therefore of little use at the peripheral level of health services, particularly when considering the additional workload involved. The low diagnostic value of these clinical signs and symptoms and other indicators in African trypanosomiasis stresses the difficulty in developing an early warning tool for an integrated control strategy in primary health care.
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PMID:[African human trypanosomiasis: study of a scoring system of presumptive diagnosis in the Congo]. 849 Sep 85

Members of the genus Trypanosoma cause African trypanosomiasis in humans and animals in Africa. Infection of mammals by African trypanosomes is characterized by an upregulation of prostaglandin (PG) production in the plasma and cerebrospinal fluid. These metabolites of arachidonic acid (AA) may, in part, be responsible for symptoms such as fever, headache, immunosuppression, deep muscle hyperaesthesia, miscarriage, ovarian dysfunction, sleepiness, and other symptoms observed in patients with chronic African trypanosomiasis. Here, we show that the protozoan parasite T. brucei is involved in PG production and that it produces PGs enzymatically from AA and its metabolite, PGH(2). Among all PGs synthesized, PGF(2alpha) was the major prostanoid produced by trypanosome lysates. We have purified a novel T. brucei PGF(2alpha) synthase (TbPGFS) and cloned its cDNA. Phylogenetic analysis and molecular properties revealed that TbPGFS is completely distinct from mammalian PGF synthases. We also found that TbPGFS mRNA expression and TbPGFS activity were high in the early logarithmic growth phase and low during the stationary phase. The characterization of TbPGFS and its gene in T. brucei provides a basis for the molecular analysis of the role of parasite-derived PGF(2alpha) in the physiology of the parasite and the pathogenesis of African trypanosomiasis.
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PMID:Identification of a novel prostaglandin f(2alpha) synthase in Trypanosoma brucei. 1106 81

Encephalopathies are the most feared complications of sleeping sickness treatment with melarsoprol. To investigate the existence of risk factors, the incidence of encephalopathic syndromes and the relationship between the development of different types of encephalopathies and the clinical outcome was studied in a clinical trial with 588 patients under treatment with melarsoprol. The 38 encephalopathy cases were classified into three types according to the leading clinical picture: coma type, convulsion type and psychotic reactions. Nine patients were attributed to the convulsion type, defined as a transient event of short duration with convulsions followed by a post-ictal phase, without signs of a generalized disease. None of these patients died from the reaction. Febrile reactions in the 48 h preceding the reaction were generally not observed in this group. Twenty-five patients were attributed to the coma type, which is a progredient coma lasting several days. Those patients often had signs of a generalized disease such as fever (84%), headache (72%) or bullous skin (8%) reactions. The risk of mortality was high in this group (52%). About 14/16 patients with encephalopathic syndrome of the coma type were infected with malaria. Patients with psychotic reactions or abnormal psychiatric behaviour (3/38) and one patient who died after alcohol intake were excluded from the analysis. The overall rate of encephalopathic syndromes in the cases analysed (n=34) was 5.8%, of which 38.2% died. We did not find any parameters of predictive value for the risk of developing an encephalopathic syndrome based on the symptoms and signs before treatment initiation. The appearance during treatment of febrile reactions (RR 11.5), headache (RR 2.5), bullous eruptions (RR 4.5) and systolic hypotension (RR 2.6) were associated with an increased risk for the occurrence of encephalopathic syndromes especially of the coma type.
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PMID:Clinical description of encephalopathic syndromes and risk factors for their occurrence and outcome during melarsoprol treatment of human African trypanosomiasis. 1134 33

A study was undertaken to investigate knowledge, attitudes and practices about sleeping sickness (human African trypanosomiasis) among communities living in and around Serengeti National Park (SENAPA). Structured questionnaires were administered to a total of 1490 consenting participants. Of the respondents, 924 (62%) knew sleeping sickness, and 807 (87.3%) knew the right place to seek healthcare. Of 924 who knew sleeping sickness, 386 (42%) said the disease was present in the areas they live. Most respondents (85.4%) knew that sleeping sickness infections were acquired in the bush and forest. The most common (69.3%) sources of information about sleeping sickness were relatives and friends. Symptoms of sleeping sickness mentioned included abnormal sleep (45.2%), fever (35.3%), body malaise (14.5%), headache (7.6%) and lymph node enlargement (6.1%). Of 1490 people interviewed 90.4% knew tsetse flies and 89.8% had been bitten by tsetse flies. The majority (86.6%) of the respondents knew that sleeping sickness is transmitted through a tsetse bite. Activities that exposed people to tsetse bites included working in tsetse infested bushes/forests, grazing livestock in tsetse infested areas and hunting game animals. In conclusion, communities living in and around SENAPA were knowledgeable about tsetse and sleeping sickness. The communities can thus understand and support community based tsetse and sleeping sickness control programmes to ensure success.
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PMID:Knowledge, attitudes and practices on tsetse and sleeping sickness among communities living in and around Serengeti National Park, Tanzania. 1825 9

Human African trypanosomiasis (HAT) or sleeping sickness is caused by the protozoan parasites Trypanosoma brucei (T.b.) gambiense (West African form) and T.b. rhodesiense (East African form) that are transmitted by the bite of the tsetse fly, Glossina spp.. Whereas most patients in endemic populations are infected with T.b. gambiense, most tourists are infected with T.b. rhodesiense. In endemic populations, T.b. gambiense HAT is characterized by chronic and intermittent fever, headache, pruritus, and lymphadenopathy in the first stage and by sleep disturbances and neuro-psychiatric disorders in the second stage. Recent descriptions of the clinical presentation of T.b. rhodesiense in endemic populations show a high variability in different foci. The symptomatology of travellers is markedly different from the usual textbook descriptions of African HAT patients. The onset of both infections is almost invariably an acute and febrile disease. Diagnosis and treatment are difficult and rely mostly on old methods and drugs. However, new molecular diagnostic technologies are under development. A promising new drug combination is currently evaluated in a phase 3 b study and further new drugs are under evaluation.
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PMID:Human African trypanosomiasis in endemic populations and travellers. 2190 32

The occurrence of coinfections in human African trypanosomiasis (HAT) patients was investigated using a retrospective data of hospital records at the National Sleeping Sickness Referral Hospital in Alupe, Kenya. A total of 31 patients, 19 males and 12 females, were diagnosed with HAT between the years 2000 and 2009. The observed co-infections included malaria (100%), helminthosis (64.5%), typhoid (22.5%), urinary tract infections (16.1%), HIV (12.9%), and tuberculosis (3.2%). The species of helminthes observed included Ancylostoma duodenale (38.7%), Ascaris lumbricoides (45.7%), Strongyloides stercoralis (9.7%), and Taenia spp. (3.2%). The patients were also infected with Entamoeba spp. (32.3%) and Trichomonas hominis (22.6%) protozoan parasites. The main clinical signs observed at the point of admission included headache (74.2%), fever (48.4%), sleep disorders (45.2%), and general body pain (41.9%). The HAT patients were treated with suramin (early stage, 9/31) and melarsoprol (late stage, 22/31). In conclusion, the study has shown that HAT patients have multiple co-infections which may influence the disease pathogenesis and complicate management of HAT.
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PMID:Prevalence and types of coinfections in sleeping sickness patients in kenya (2000/2009). 2191 84

The number of imported Human African Trypanosomiasis (HAT) cases in non-endemic countries has increased over the last years. The objective of this analysis is to describe the clinical presentation of HAT in Caucasian travelers. Literature was screened (MEDLINE, Pubmed) using the terms "Human African Trypanosomiasis", "travelers" and "expatriates"; all European languages except Slavic ones were included. Publications without clinical description of patients were only included in the epidemiological analysis. Forty-five reports on Caucasians with T.b. rhodesiense and 15 with T.b. gambiense infections were included in the analysis of the clinical parameters. Both species have presented with fever (T.b. rhodesiense 97.8% and T.b. gambiense 93.3%), headache (50% each) and a trypanosomal chancre (T.b. rhodesiense 84.4%, T.b. gambiense 46.7%). While sleeping disorders dominate the clinical presentation of HAT in endemic regions, there have been only rare reports in travelers: insomnia (T.b. rhodesiense 7.1%, T.b. gambiense 21.4%), diurnal somnolence (T.b. rhodesiense 4.8%, T.b. gambiense none). Surprisingly, jaundice has been seen in 24.2% of the Caucasian T.b. rhodesiense patients, but has never been described in HAT patients in endemic regions. These results contrast to the clinical presentation of T.b. gambiense and T.b. rhodesiense HAT in Africans in endemic regions, where the presentation of chronic T.b. gambiense and acute T.b. rhodesiense HAT is different. The analysis of 14 reports on T.b. gambiense HAT in Africans living in a non-endemic country shows that neurological symptoms such as somnolence (46.2%), motor deficit (64.3%) and reflex anomalies (14.3%) as well as psychiatric symptoms such as hallucinations (21.4%) or depression (21.4%) may dominate the clinical picture. Often, the diagnosis has been missed initially: some patients have even been hospitalized in psychiatric clinics. In travelers T.b. rhodesiense and gambiense present as acute illnesses and chancres are frequently seen. The diagnosis of HAT in Africans living outside the endemic region is often missed or delayed, leading to presentation with advanced stages of the disease.
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PMID:Sleeping sickness in travelers - do they really sleep? 2206 3

Cerebral involvement in parasitoses is an important clinical manifestation of most of the human parasitoses. Parasites that have been described to affect the central nervous system (CNS), either as the dominant or as a collateral feature, include cestodes (Taenia solium (neurocysticerciasis), Echinococcus granulosus (cerebral cystic echinococcosis), E. multilocularis (cerebral alveolar echinococcosis), Spirometra mansoni (neurosparganosis)), nematodes (Toxocara canis and T. cati (neurotoxocariasis), Trichinella spiralis (neurotrichinelliasis), Angiostrongylus cantonensis and A. costaricensis (neuroangiostrongyliasis), Gnathostoma spinigerum (gnathostomiasis)), trematodes (Schistosoma mansoni (cerebral bilharziosis), Paragonimus westermani (neuroparagonimiasis)), or protozoa (Toxoplasma gondii (neurotoxoplasmosis), Acanthamoeba spp. or Balamuthia mandrillaris (granulomatous amoebic encephalitis), Naegleria (primary amoebic meningo-encephalitis), Entamoeba histolytica (brain abscess), Plasmodium falciparum (cerebral malaria), Trypanosoma brucei gambiense/rhodesiense (sleeping sickness) or Trypanosoma cruzi (cerebral Chagas disease)). Adults or larvae of helminths or protozoa enter the CNS and cause meningitis, encephalitis, ventriculitis, myelitis, ischaemic stroke, bleeding, venous thrombosis or cerebral abscess, clinically manifesting as headache, epilepsy, weakness, cognitive decline, impaired consciousness, confusion, coma or focal neurological deficits. Diagnosis of cerebral parasitoses is dependent on the causative agent. Available diagnostic tools include clinical presentation, blood tests (eosinophilia, plasmodia in blood smear, antibodies against the parasite), cerebrospinal fluid (CSF) investigations, imaging findings and occasionally cerebral biopsy. Treatment relies on drugs and sometimes surgery. Outcome of cerebral parasitoses is highly variable, depending on the effect of drugs, whether they are self-limiting (e.g. Angiostrongylus costaricensis) or whether they remain undetected or asymptomatic, like 25% of neurocysticerciasis cases.
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PMID:Parasitoses of the human central nervous system. 2304 8


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