Gene/Protein
Disease
Symptom
Drug
Enzyme
Compound
Pivot Concepts:
Gene/Protein
Disease
Symptom
Drug
Enzyme
Compound
Target Concepts:
Gene/Protein
Disease
Symptom
Drug
Enzyme
Compound
Query: UMLS:C0023380 (
lethargy
)
5,697
document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)
A 34-year-old woman was hospitalised with hypotension,
lethargy
and ventricular tachycardia, five months after an uneventful pregnancy and delivery. Laboratory values were compatible with anterior (abnormal concentrations of adrenocorticotropin hormone, thyroid stimulating hormone, prolactin) and posterior (diabetes insipidus) pituitary gland insufficiency. An
MRI
scan revealed that there was no pituitary enlargement and that the pituitary stalk was normal. The prompt recognition of hypophysitis as a potentially fatal condition is important, as a life-saving treatment is available.
...
PMID:[Clinical thinking and decision making in practice. A patient with postpartum malaise, anorexia, and ventricular tachycardia]. 1177 Feb 65
A 64-year-old woman presented with sudden onset of disequilibrium and dysarthria. Two days later she became
lethargic
and tetraparetic. An emergency
MRI
disclosed multiple infarctions in the medulla oblongata and pons. An angiogram revealed severe stenosis of the rostral basilar artery. The patient underwent a rapidly progressive course with impaired consciousness and flaccid tetraplegia. MR images 7 days after the onset disclosed a symmetrical midbrain infarction that was localized mainly in the cerebral peduncles, suggesting a distal basilar artery occlusion as the cause of this pathology. Since 4 weeks after the onset the patient was in the persistent vegetative state, which was essentially unchanged during the 1-year follow-up period. Persistent vegetative state is known to be caused by diffuse supratentorial or bilateral thalamic lesions, but in our case the lesions were restricted to the infratentorial area. We speculate a mechanism to cause the persistent vegetative state by partial impairment of the connection to the thalamic ascending system or extrathalamic ascending system, which leads to the dissociation of arousal(preserved in this case) and awareness(impaired in this case) after the ventral midbrain infarction.
...
PMID:[A case of the persistent vegetative state following symmetrical peduncular infarction]. 1186 54
An epidemic of enterovirus 71 (EV71) infection compatible with hand, foot and mouth disease and associated with high morbidity and mortality occurred in Taiwan in 1998. We recruited 90 patients (50 males, 40 females) with definite EV71 infections for clinical and laboratory analysis. The neurological signs and symptoms, all of which occurred during the febrile period, in patients with central nervous system (CNS) involvement (aseptic meningitis, encephalitis or myelitis) were myoclonic jerks (23/33), vomiting (10/33), ataxia (7/33),
lethargy
(6/33), seizure (4/33) and tremor (2/33). Patients with CNS involvement had longer durations of fever (4.6+/-0.2 vs. 3.1+/-0.3 d; p <0.01) and a higher white blood cell count (12,512+/-658 vs. 10,607+/-409 cells/mm3; p = 0.01) than patients without CNS involvement. The case fatality rate in patients with CNS involvement was 4/33 (12%), whereas no fatalities (0/57) occurred in patients without CNS involvement. Six of 11 patients subjected to
MRI
showed a high intensity T2-weighted signal in the brainstem. A nested fluorescent RT-PCR for detection of virus in throat and stool specimens showed higher sensitivity than viral culture. Viremia was detectable using RT-PCR in 20% of cases (3/15), whereas no virus was isolated from culture or detected by RT-PCR in cerebrospinal fluid.
...
PMID:Clinical manifestations and laboratory assessment in an enterovirus 71 outbreak in southern Taiwan. 1192 38
We report an infant with intermittent urinary excretion of D-2-hydroxyglutaric (D-2-OHG) acid who died at the age of 10 months from cardiogenic shock due to cardiomyopathy. High urinary concentrations of D-2-OHG and succinic acid, as well as increased levels of lactic acid were detected on three different occasions, whereas a normal urinary profile of organic acids was found on one occasion. The clinical findings of our patient consisted of generalized hypotonia, irritability, developmental delay, generalized tonic seizures,
lethargy
, cardiomyopathy, and respiratory distress. Cerebral
MRI
revealed bilateral lesions in the substantia nigra, the periaqueductal area, the medial part of the thalamus, the hypothalamus, the caudate nucleus, putamen and globus pallidus. This pattern is suggestive of a mitochondriopathy. However, respiratory chain enzyme activities were normal in fibroblasts. Exogenous supplementation of D-2-OHG acid strongly inhibited cytochrome-c oxidase activity in fibroblasts from the patient and from normal controls in vitro. The results suggest that our patient has an unusual form of D-2-hydroxyglutaric aciduria (D-2-OHGA), different from the patients published so far, and that the increase of lactic acid and some citric acid cycle intermediates encountered in some patients with D-2-OHGA may be due to a functional defect of the respiratory chain caused by D-2-OHG acid.
...
PMID:D-2-Hydroxyglutaric aciduria in a patient with a severe clinical phenotype and unusual MRI findings. 1199 77
Experimental occlusion of the middle cerebral artery and the reduction of cerebral blood flow (CBF) below 15 ml/100 gm/per minute cause failure of the somatosensory evoked response and
lethargy
of cortical neurones. Increase of CBF to normal value normalises the bioelectrical activity within the "penumbra"--the zone surrounding the necrotic area. In this "risk zone" neurones can survive only a few hours. So the penumbra is a "therapeutic window" in which therapy can save some neurones from death. However, if decrease of CBF is continued, numerous cells within the penumbra gradually die. The phenomenon of the penumbra, based on experiments, was applied to human ischaemic stroke; however great differences between experimental and human brain ischaemia do exist. The human course of disease and the size of necrotic lesion depend on numerous additional factors. The three very important critical values of CBF which decrease in human brain ischaemia are difficult to examine. New imaging methods play a great diagnostic role in searching for the penumbra, but their diagnostic possibilities and results are limited. In the short-time duration of the therapeutic window both CT and
MRI
often do not indicate ischaemic lesion. So, it is not known whether the penumbra is present or not. Conclusive estimation of
MRI
diffusion-weighted imaging and perfusion-imaging and of their coefficient is impossible to obtain in the time exceeding the "therapeutic window'" Numerous additional various diseases and compensatory vascular mechanisms influence the necrotic zone in human focal ischaemia. Probably for this reason a difficulty in the estimation of the penumbra in human is observed. So, it seems that the penumbra--the therapeutic window or risk zone--in human probably occurs only in some cases. It may be one of numerous reasons for the limited effectiveness of ischaemic stroke therapy. It is not known when the penumbra is overspread with oedema, which always appears to a greater or a lesser degree. Maybe the efforts of experimental investigators, physicians and pharmacologists should also be taken into consideration to find drugs decreasing oedema and BBB permeability.
...
PMID:Experimental and human ischaemia: is the penumbra present in human ischaemic stroke? 1257 78
We report on the case of a 20 year old woman with no previous psychiatric history, who displayed a first episode of catatonia with acute onset. Symptoms started plainly with sudden general impairment, intense asthenia, headache, abdominal pain and confusion. After 48 hours, the patient was first admitted to an emergency unit and transferred to an internal medicine ward afterwards. She kept confused. Her behaviour was bizarre with permanent swinging of pelvis, mannerism, answers off the point and increasingly poor. The general clinical examination was normal, except for the presence of a regular tachycardia (120 bpm). The paraclinical investigations also showed normal: biology, EEG, CT Scan, lumbar puncture. Confusion persisted. The patient remained
stuporous
, with fixed gazing and listening-like attitudes. She managed to eat and move with the help of nurses but remained bedridden. The neurological examination showed hypokinaesia, extended hypotonia, sweating, urinary incontinence, bilateral sharp reflexes with no Babinski's sign and an inexhaustible nasoorbicular reflex. The patient was mute and contrary, actively closed her eyes, but responded occasionally to simple instructions. For short moments, she suddenly engaged in inappropriate behaviors (wandering around) while connecting back to her environment answering the telephone and talking to her parents. The patient's temperature rose twice in the first days but with no specific etiology found. During the first 8 days of hospitalization, an antipsychotic treatment was administered: haloperidol 10 mg per os daily and cyamemazine 37.5 mg i.m. daily. Despite these medications, the patient worsened and was transferred to our psychiatric unit in order to manage this catatonic picture with rapid onset for which no organic etiology was found. On admission, the patient was
stuporous
, immobile, unresponsive to any instruction, with catalepsy, maintenance of postures, severe negativism and refusal to eat. A first treatment by benzodiazepine (clorazepate 20 mg i.v.) did not lead to any improvement. The organic investigations were completed with cerebral
MRI
and the ruling out of a Wilson's disease. Convulsive therapy was then decided. It proved dramatically effective from the first attempt; 4 shocks were carried out before the patient's relatives ask for her discharge from hospital. The patient revealed she had experienced low delirium during her catatonic state. The clinical picture that followed showed retardation with anxiety. She was scared with fear both for the other patients and the nursing team. She kept distant and expressed few affects. The treatment at the time of discharge was olanzapine 10 mg per os. She was discharged with a diagnosis of catatonia but with no specific psychiatric etiological diagnosis associated. She discontinued her follow-up a few weeks later. After one year, we had no information about her. Catatonia has now become rare but remains a problem for clinicians. We reviewed data concerning short term vital prognosis and psychiatric long term prognosis in catatonia. Lethal catatonia is associated with acute onset, both marked psychomotor and neurovegetative symptoms. In the light of literature, there is no proband clinical criterion during the episode that is of relevant diagnostic value to ascertain the psychiatric etiology.
...
PMID:[Catatonia de novo, report on a case: immediate vital prognosis and psychiatric prognosis in longer term]. 1264 Mar 30
A case of pilocytic astrocytoma of neurohypophysis is presented. The clinical, pathological and
MRI
features of a rare tumor of the neurohypophysis are described. A 5-year-old girl presented with a 3 month history of
lethargy
, imbalance and visual disturbances. A
MRI
revealed a large suprasellar mass. Histopathological examination demonstrated a pilocytic astrocytoma. Its astrocytic nature was confirmed by positive immunostaining for GFAP and the findings of an electron microscopy.
...
PMID:Pilocytic astrocytoma of neurohypophysis. 1457 Feb 90
In 1916, von Economo first described encephalitis lethargica (EL), a CNS disorder presenting with pharyngitis followed by sleep disorder, basal ganglia signs (particularly parkinsonism) and neuropsychiatric sequelae. Since the 1916-1927 epidemic, only sporadic cases have been described. Pathological studies revealed an encephalitis of the midbrain and basal ganglia, with lymphocyte (predominantly plasma cell) infiltration. The EL epidemic occurred during the same time period as the 1918 influenza pandemic, and the two outbreaks have been linked in the medical literature. However, von Economo and other contemporary scientists thought that the 1918 influenza virus was not the cause of EL. Recent examination of archived EL brain material has failed to demonstrate influenza RNA, adding to the evidence that EL was not an invasive influenza encephalitis. By contrast, the findings of intrathecal oligoclonal bands (OCB) and beneficial effects of steroid treatments have provoked the hypothesis that EL may be immune-mediated. We have recently seen 20 patients with a similar EL phenotype, 55% of whom had a preceding pharyngitis. The patients had remarkable similarity to the historical descriptions of EL: sleep disorder (somnolence, sleep inversion or insomnia),
lethargy
, parkinsonism, dyskinesias and neuropsychiatric symptoms. CSF examination commonly showed elevated protein and OCB (75 and 69% respectively). Investigation found no evidence of viral encephalitis or other recognized causes of rapid-onset parkinsonism.
MRI
of the brain was normal in 60% but showed inflammatory changes localized to the deep grey matter in 40% of patients. We investigated the possibility that this phenotype could be a postinfectious autoimmune CNS disorder, and therefore similar to Sydenham's chorea. Anti-streptolysin-O titres were elevated in 65% of patients. Furthermore, western immunoblotting showed that 95% of EL patients had autoantibodies reactive against human basal ganglia antigens. These antibodies were also present in the CSF in four patients tested. By contrast, antibodies reactive against the basal ganglia were found in only 2-4% of child and adult controls (n = 173, P < 0.0001). Rather than showing polyspecific binding, these antibodies bound to common neural autoantigens of molecular weight 40, 45, 60 and 98 kDa. Regional tissue comparisons showed that the majority of these autoantigens were specific to or enriched in CNS tissue. Immunohistochemistry with secondary staining localized antibody binding to neurons rather than glial populations. Further investigation is required to determine whether these antibodies affect neuronal function (i.e. whether they are pathogenic anti-neuronal antibodies). Histopathology in one case demonstrated striatal encephalitis with perivenous B- and T-lymphocytic infiltration. We believe an EL-like syndrome is still prevalent, and propose that this syndrome may be secondary to autoimmunity against deep grey matter neurons.
...
PMID:Encephalitis lethargica syndrome: 20 new cases and evidence of basal ganglia autoimmunity. 1467 31
Reversible posterior leukoencephalopathy syndrome (RPLS) was described by Hinchey and colleagues in 1996. The disorder occurs predominantly in patients with acute hypertension and/or on pharmacological immunosuppression. We report a 6-year-old male with cerebral X-linked adrenoleukodystrophy who received an HLA-matched unrelated bone marrow transplant (BMT). Cyclosporine was used as graft-versus-host disease prophylaxis. At 55 days post-BMT, his cyclosporine concentrations were high for several days and the concentration was still high on day 70 (353 microg/L). He presented 83 days post-BMT with new onset of headache,
lethargy
, acute visual loss and focal seizures. He was not hypertensive.
MRI
of the head revealed signal changes that now extended more peripherally into the subcortical and cortical regions of the occipital and temporal lobes. The patient's cyclosporine was stopped for 5 days. The patient's vision returned to normal and his headaches and
lethargy
resolved with no further seizures 3 weeks later. Follow-up
MRI
of the head 2 months later showed almost complete resolution of the cortical signal abnormalities. It is important to consider RPLS in patients with cerebral adrenoleukodystrophy who present with acute neurological deterioration. Attention to the pattern of white matter and the presence of cortical grey matter involvement on neuroimaging is important for the diagnosis. When appropriate management is initiated, that is controlling hypertension when present and discontinuing or reducing the dose of offending immunosuppressive agents, the acute neurological symptoms will usually resolve.
...
PMID:Reversible posterior leukoencephalopathy syndrome in a child with cerebral X-linked adrenoleukodystrophy treated with cyclosporine after bone marrow transplantation. 1460 98
A 74-year-old woman presented with progressive mental deterioration following a low-grade fever and headache. Upon admission, she appeared
lethargic
, could not obey simple commands and was disoriented to time, place and person. She had low-grade fever and mild neck stiffness. The cerebrospinal fluid had an elevated protein content of 496 mg/dl, contrast-enhanced
MRI
revealed diffuse leptomeningeal enhancement, particularly in the occipital area, and a cerebral angiogram showed diffuse segmental narrowing of multiple intracranial arteries, especially in the distal portion of the right middle cerebral artery. A clinical diagnosis of granulomatous angiitis of the central nervous systems (GANS) was made, and corticosteroid therapy was initiated. The patient improved gradually, and corticosteroid therapy was tapered to the maintenance dose (prednisolone 0.4 mg/kg daily). An open brain biopsy showed multiple vessels containing granulomatous inflammation with giant cells. GANS is one of the most challenging neurologic disorders to diagnose because of its relative rarity and the lack of specificity of clinical signs and efficient, non-invasive, diagnostic tests. In this case, we were able to begin corticosteroid therapy in the early stage of the disease (before brain biopsy), and it yielded a good outcome.
...
PMID:[Successful early-stage corticosteroid treatment in a case of granulomatous angiitis of the central nervous system]. 1465 5
<< Previous
1
2
3
4
5
6
7
8
9
10
Next >>