Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UMLS:C0023380 (lethargy)
 5,697 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

We reviewed the clinical, neuroradiological, and serological findings in 27 patients with cerebral toxoplasmosis complicating the acquired immune deficiency syndrome, 19 of whom were also analyzed neuropathologically. The clinical manifestations of this disorder varied, ranging from headache and fever to coma. However, the characteristic presentation included focal neurological symptoms and signs, usually of subacute onset. In addition, two-thirds of the patients exhibited more generalized cerebral dysfunction with confusion and lethargy. The computed tomographic (CT) scan most commonly revealed ring contrast enhancement, which appeared to correlate best with the histological presence of vascular proliferation and inflammation surrounding the abscesses. However, in 5 patients the CT scan revealed either homogeneous enhancement or no enhancement, and in 3 patients the scans were negative. In general, CT scans underrepresented the number of lesions eventually documented pathologically. Double-dose contrast administration and preliminary experience with magnetic resonance imaging suggested that these techniques were superior to standard CT scanning in detecting Toxoplasma lesions. All patients were seropositive for IgG antibody against Toxoplasma gondii in blood, both before the onset of illness and at the time of presentation, although titers in some patients were as low as 1:8 and most patients did not exhibit rising titers. Prompt therapy resulted in rapid clinical improvement, documented by CT scan, associated with the development of an organizing tissue response in the host and elimination of free organisms. Response to treatment was sufficiently rapid in most patients to allow a trial of therapy as the favored approach to diagnosis.
 ...
PMID:Cerebral toxoplasmosis complicating the acquired immune deficiency syndrome: clinical and neuropathological findings in 27 patients. 396 67

We presented a case of Creutzfeldt-Jakob disease (CJD) associated with ocular dipping (OD). A 65-year-old woman was hospitalized with two months history of progressive ataxia and mental deterioration. On admission, she was bed-ridden and stuporous with rigidity of the four limbs. Her both eyes were noted to deviate downward slowly from midpossition, taking 1 to 3 seconds to reach the nadir and rapidly returned to midpossition. It was felt that these abnormal eye movements are compatible with OD. Findings of EOG were compatible with that of typical OD. Electroencephalogram obtained a few months later revealed periodic synchronous discharge. Magnetic resonance imaging of the brain which had demonstrated mild cerebral atrophy in the beginning subsequently revealed full-brown cerebral atrophy. Hence, she was diagnosed of having CJD. There has been no report of CJD associated with OD. The OD was observed to last as long as 110 days. When the above described abnormal eye movements were noted, there was no signs indicative of brain stem dysfunction present. Therefore, we feel that the present case suggest that a diffuse cerebral dysfunction involving the cerebral cortex and basal ganglia may underlie in the development of OD.
 ...
PMID:[Creutzfeldt-Jakob disease associated with ocular dipping--a case report]. 959 17

Hyperargininemia is a metabolic disorder biochemically characterized by tissue accumulation of arginine (Arg) and other guanidino compounds (GC). Convulsions, lethargy and psychomotor delay are predominant clinical features of this disease. Considering that some GC are epileptogenic and cause a decrease in membrane fluidity and that Na+,K(+)-ATPase, a membrane-bound enzyme, is essential for cellular excitability and is decreased in experimental and human epilepsy, in the present study we determined the in vitro effects of Arg, N-acetylarginine (NAA), argininic acid (AA) and homoarginine (HA) on the activity of Na+,K(+)-ATPase in the synaptic plasma membrane from cerebral cortex of young rats in the hope to identify a possible mechanism for the brain damage in hyperargininemia. The results showed that all GC tested, except Arg, significantly inhibited Na+,K(+)-ATPase activity at concentrations similar to those observed in plasma and CSF of patients with hyperargininemia. In addition, competition between NAA, AA and HA for the binding to the enzyme was observed, suggesting a common binding site for the GC. It is therefore possible that the inhibitory effect of GC on Na+,K(+)-ATPase may be related to the brain dysfunction observed in hyperargininemia.
 ...
PMID:In vitro inhibition of Na+,K(+)-ATPase activity from rat cerebral cortex by guanidino compounds accumulating in hyperargininemia. 1044 19

Hyperargininemia is a metabolic disorder biochemically characterized by tissue accumulation of arginine and other guanidino compounds. Convulsions, lethargy and psychomotor delay or cognitive deterioration are predominant clinical features of this disease. Although neurologic symptoms predominate in this disorder, their pathophysiology is still unknown. In the present study we investigated the in vitro effects of arginine, N-acetylarginine, argininic acid and homoarginine on some oxidative stress parameters in rat brain in the hope to identify a possible mechanism for the brain damage in hyperargininemia. Chemiluminescence, total radical-trapping antioxidant potential (TRAP), superoxide dismutase (SOD), catalase (CAT) and glutathione peroxidase (GSH-Px) activities were measured in the cerebral cortex of rats in the presence of various concentrations of these compounds. The results showed that all guanidino compounds tested significantly increased chemiluminescence and decreased TRAP at concentrations similar to those observed in the tissue of hyperargininemic patients. Furthermore, these compounds inhibited CAT and GSH-Px activities to varying extents, with GSH-Px activity being more susceptible to their action. In turn, argininic acid inhibited all enzyme activities, and its main action was also directed towards GSH-Px. The results suggest that oxidative stress caused by guanidino compounds may be involved in the brain dysfunction amongst other potential pathophysiological mechanisms observed in hyperargininemia.
 ...
PMID:In vitro stimulation of oxidative stress in cerebral cortex of rats by the guanidino compounds accumulating in hyperargininemia. 1174 72

Migraine is a reversible brain dysfunction characterized by pain and passive coping strategies consistent with sickness behaviour. The brain contains no pain fibres and the only way it may signal pain is through the trigemino-vascular system. Here, it is postulated that migraine is an example of genetically determined behavioural responses and that sickness behaviour, a pan-mammalian adaptive response to internal and external stressors, characterizes the migraine attacks. Sickness behaviour is manifested in withdrawal and motor quiescence, sympatho-inhibition and lethargy, in which visceral pain signals a homeostatic imbalance of the brain. The sickness behavioural response is associated to pain felt as inescapable visceral pain, and depends upon brain networks involving different brainstem, hypothalamus and forebrain regions, that encode evolutionarily conserved adaptive genetic responses. This hypothesis, still speculative, may offer a more coherent view of migraine as an adaptive biobehavioural response triggered by a threatened brain.
 ...
PMID:Migraine as a visceral pain. 1941 20