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Query: UMLS:C0024530 (malaria)
 44,886 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

This paper reviews the neurological complications of malaria. Cerebral malaria, the acute encephalopathy which complicates exclusively the infection by Plasmodium falciparum commonly affects children and adolescents in hyperendemic areas. Plugging of cerebral capillaries and venules by clumped, parasitized red blood cells causing blood sludging in the capillary circulation is one hypothesis to explain its pathogenesis. The other is a humoral hypothesis which proposes a nonspecific, immune-mediated, inflammatory response with release of vasoactive substances capable of producing endothelial damage and alterations of permeability. Cerebral malaria has a mortality rate up to 50%, and also a considerable longterm morbidity, particularly in children. Hypoglycemia, largely in patients treated with quinine, may complicate the cerebral symptomatology. Other central nervous manifestations of malaria include intracranial hemorrhage, cerebral arterial occlusion, and transient extrapyramidal and neuropsychiatric manifestations. A self-limiting, isolated cerebellar ataxia, presumably caused by immunological mechanisms, in patients recovering from falciparum malaria has been recognized in Sri Lanka. Malaria is a common cause of febrile seizures in the tropics, and it also contributes to the development of epilepsy in later life. Several reports of spinal cord and peripheral nerve involvement are also available. A transient muscle paralysis resembling periodic paralysis during febrile episodes of malaria has been described in some patients. The pathogenesis of these neurological manifestations in malaria remains unexplored, but offers excellent perspectives for research at clinical as well as experimental level.
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PMID:Neurological complications of malaria. 129 73

The involvement of the nervous system in malaria is reviewed in this paper. Cerebral malaria, the acute encephalopathy which complicates exclusively the infection by Plasmodium falciparum commonly affects children and adolescents in hyperendemic areas. Plugging of cerebral capillaries and venules by clumped, parasitized red cells causing sludging in the capillary circulation is one hypothesis to explain its pathogenesis. The other is a humoral hypothesis which proposes nonspecific, immune-mediated, inflammatory responses with release of vasoactive substances capable of producing endothelial damage and alterations of permeability. Cerebral malaria has a mortality rate up to 50%, and also a considerable longterm morbidity, particularly in children. Hypoglycemia, largely in patients treated with quinine, may complicate the cerebral symptomatology. Other central nervous manifestations of malaria include intracranial hemorrhage, cerebral arterial occlusion, and transient extrapyramidal and neuropsychiatric manifestations. A self-limiting, isolated cerebellar ataxia, presumably caused by immunological mechanisms, in patients recovering from falciparum malaria has been recognized in Sri Lanka. Malaria is a common cause of febrile seizures in the tropics, and it also contributes to the development of epilepsy in later life. Several reports of spinal cord and peripheral nerve involvement are also available. A transient muscle paralysis resembling periodic paralysis during febrile episodes of malaria has been described in some patients. The pathogenesis of these neurological manifestations remains unexplored, but offers excellent perspectives for research at a clinical as well as experimental level.
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PMID:Neurological manifestations of malaria. 130 75

Evidence for immune activation was investigated in 12 patients with a rare syndrome of self-limiting, delayed onset cerebellar dysfunction following an attack of falciparum malaria which occurred 18-26 d previously. Concentrations of tumour necrosis factor, interleukin 6 and interleukin 2 were all significantly higher in serum samples of patients during cerebellar ataxia than in recovery sera and in the sera of 8 patients who did not develop delayed cerebellar dysfunction following an attack of falciparum malaria. Cytokine concentrations in the cerebrospinal fluid were also significantly higher in ataxic patients than in controls. These findings suggest that immunological mechanisms may play a role in delayed cerebellar dysfunction following falciparum malaria.
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PMID:Immune activation during cerebellar dysfunction following Plasmodium falciparum malaria. 144 Jul 67

A 6-month-old Miniature Doberman Pinscher was presented with inappetance and cerebellar signs. Babesia canis organisms were found on a capillary bloodsmear. The cerebellar signs resolved rapidly following treatment with diminazene aceturate. A 7-month-old Siberian Husky developed cerebellar signs, blindness and quadriparesis 9 d after presentation with clinical signs typical of uncomplicated canine babesiosis. The dog responded favourably to treatment with prednisolone. Both acute and delayed cerebellar ataxia have been associated with malaria in humans. The clinical signs shown by these dogs were similar to those reported for malaria in humans. Cerebellar ataxia should be considered a possible complication of canine babesiosis.
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PMID:Cerebellar ataxia as a possible complication of babesiosis in two dogs. 759 21

Immunological mechanisms have been implicated in the pathogenesis of delayed cerebellar ataxia following falciparum malaria (DCA). We tested serum and CSF samples obtained from 39 Sri Lankan patients with DCA for the presence of antibodies (Ab) directed against cerebellar Purkinje cells by an immunofluorescence (IF) technique and Western blot analysis. For the IF test 7 mu thick frozen sections of histologically normal cerebellum obtained at post mortem were used. Proteins obtained from crude preparations of Purkinje cells isolated from the cerebellum were used for Western blot analysis. Sera obtained from patients known to have antineuronal antibodies associated with cerebellar degenerations and paraneoplastic disorders (anti-Hu and anti-Yo Ab) and sera from normal blood donors served as positive and negative controls, respectively. All serum and CSF samples obtained from patients with DCA were negative for Ab directed against cerebellar Purkinje cells. Humoral mechanisms are, therefore, unlikely to be important in the pathogenesis of this delayed complication of falciparum malaria.
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PMID:Absence of anti-Purkinje cell antibodies in patients with cerebellar ataxia following falciparum malaria. 766 18

We report the clinical features of 74 patients with delayed cerebellar ataxia (DCA) following falciparum malaria, who were prospectively followed up at two centres. This unusual complication has an acute onset, with signs suggesting a predominantly midline cerebellar lesion without any evidence of cerebral involvement. There was a delay of a median 13 days between the onset of fever and the onset of ataxia. DCA has a good prognosis, with spontaneous and complete recovery within 3 months. In our opinion, it is an example of a post-infective neurological syndrome possibly mediated via an immune mechanism.
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PMID:Delayed cerebellar ataxia complicating falciparum malaria: a clinical study of 74 patients. 793 48

Infections with malaria are increasing in Europe and Northern America and are also spreading in tropical endemic areas. A falciparum variety of malaria known as cerebral malaria is the most well-known neurological complication, caused by Plasmodium falciparum and characterised by a fulminant course with disturbances of consciousness and facultative seizures or focal neurological deficits. 50% of deaths caused by malaria are due to cerebral involvement. Pathologically a disseminated vasculomyelinopathic disorder is seen. Immunological changes, vascular-hypoxic disturbances and metabolic-toxic factors contribute to these pathological findings. Facts on diagnostic, differential diagnostic and therapeutic procedures are presented. Beside the severe and life-threatening cerebral malaria some unspecific cerebral symptoms are seen, such as cerebellar ataxia and chorea. Spinal disease and peripheral nerve involvement, polyradiculitis and especially psychiatric disorders have also been described. Every neurological and psychiatric disorder presented first in tropical areas or malaria-endemic regions requires malaria diagnostic tests. In our geographical region, any previous history of a journey to the tropics is an important pointer; in particular, neurological or psychiatric symptoms can be important pointers to malaria.
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PMID:[Neurologic complications of malaria infection]. 844 77

This hospital based study was carried out on 185 adult patients of cerebral malaria. Out of 185 patients, 62 (33.5%) died and 123 (66.5%) survived. Neurological sequelae were present in 13 (10.5%) of 123 survivors at the time of discharge (i.e. 10-15 days after recovery from coma) from the hospital. These were in form of psychosis in 5 patients (4%), cerebellar ataxia in 4 patients (3.2%), extrapyramidal rigidity in 2 patients (1.62%) and hemiplegia in 2 patients (1.62%).
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PMID:Incidence and outcome of neurological sequelae in survivors of cerebral malaria. 925 38

Cerebellar ataxia is an unusual post malarial complication. We encountered 10 patients of this disease (3 in 1992 and 7 in 1994) during the malaria epidemic period in Bikaner, Rajasthan. All patients were permanent residents to malaria endemic areas. The ataxic symptoms appeared after an afebrile period of 2-7 days. The neurological examination revealed no other abnormality except a cerebellar syndrome interfering with normal gait and speech. Lower limbs were affected more than the upper limbs and the mean delay between onset of fever and onset of cerebellar ataxia was 13 days. Peripheral blood film of all cases showed gametocytes of Plasmodium falciparum and in two cases schizonts of the same. All the patients improved within one month without any residual deficit. Further follow up for next 4 weeks revealed no abnormality.
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PMID:Delayed cerebellar ataxia--a complication of Plasmodium falciparum malaria. 925 40

32 cases (21 acute severe malaria and 11 chronic malaria syndrome), who developed unusual complications and/or manifestations are reported. The acute manifestations were unexplained tachypnoea 4, pulmonary oedema 5 and shock due to multiple organ dysfunction syndrome 3, melena 2 and E coli septicaemia in one. The other features were concomitant salmonellosis 2, meningitis 1, renal failure 3, hepatorenal syndrome 2, hepatitis like illness 7, neck stiffness with normal CSF 3, urticaria and subconiunctival haemorrhage 2 each, apyrexial spell with anaemia 4, thromocytopenia 3, and hypoglycaemia 3 (two pretreatment and one while on quinine in 5% glucose drip). The chronic syndrome noted were hyperreactive malaria syndrome (Tropical splenomegaly) 3, repeated haemolysis 2, chronic simple malaria with positive parasitaemia and normal Igm levels 4, and cerebellar ataxia with tremors 3. Bone marrow in these cases was hypercullular with increase plasma cells. Liver biopsy revealed lymphocytic infiltration. There was no case with permanent neurogical deficit. All patients with pulmonary oedema and multiple organ dysfunction died but chronic syndrome patients recovered fully. Early recoginition of atypical manifestation and prompt treatment will decrease the mortality and morbidity due to malaria.
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PMID:Unusual acute and chronic complications of malaria. 928 1


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