Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0011570 (depression)
 172,036 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Here we report the clinical and pathological findings in a 30-year-old drug addict in whom an intravenous injection of heroin led to reversible coma with respiratory depression and heart failure. On regaining consciousness, the patient was found to have rhabdomyolysis with renal failure requiring dialysis and peripheral neuropathy. Three weeks later his neurological condition suddenly deteriorated and delayed encephalopathy developed, leading to death 20 days later. The neuropathological study of the brain disclosed pale, spongy myelin with diffuse reactive astrogliosis and microglial proliferation, without hypoxic necrotic lesions. The cerebral and cerebellar cortices were unchanged. The absence of typical hypoxic lesions and the presence of spongiosis with massive astrocytosis distinguished this case from the previously reported cases of delayed leukoencephalopathy following severe hypoxia. An immunocytochemical study designed to exclude an underlying alteration of the metabolic oxidative pathway detected normal expression of the respiratory chain complexes IV, III and V. Despite the absence of an oxidative chain alteration in our patient, we cannot exclude the possibility that an individual predisposition played a pathogenetic role in this delayed leukoencephalopathy.
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PMID:Delayed spongiform leukoencephalopathy after heroin abuse. 922 35

Numerous studies suggest that modifications in concentrations of both excitatory and inhibitory amino acids are implicated in the pathophysiology of portal-systemic encephalopathy (PSE), a neuropsychiatric disorder associated with chronic liver disease in humans. In this study, amino acid levels were measured by High Performance Liquid Chromatography (HPLC) in Cerebrospinal Fluid (CSF) of 10 dogs (age range: 3 mo.- 3 yr 4 mo.) exhibiting a congenital portal-systemic shunt, either intra or extra-hepatic, and 8 age-matched control dogs who showed no signs of hepatic or neurologic disorders. Dogs with congenital shunts manifested signs of encephalopathy such as disorientation, head pressing, vocalization, depression, seizures and coma. CSF from dogs with congenital shunts contained significantly increased amounts of glutamate (2 to 3-fold increase, p<0.01), glutamine (6-fold increase, p<0.05) and aromatic amino acids (phenylalanine, tyrosine and tryptophan) compared to CSF of control dogs. Concentrations of GABA and branched chain amino acids (valine, leucine, isoleucine) were within normal limits. Modifications of brain glutamate (an excitatory amino acid) as well as tryptophan (the precursor of serotonin) could contribute to the neurological syndrome characteristic of congenital PSE in dogs.
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PMID:Selective alterations of cerebrospinal fluid amino acids in dogs with congenital portosystemic shunts. 947 3

A patient with severe and protracted symptoms from intracranial hypotension is described. The patient's presentation was marked by diffuse encephalopathy and profound depression of consciousness. This case report expands the presently known clinical spectrum of this uncommon and generally benign illness. The clinical and laboratory findings typically observed in the syndrome of intracranial hypotension are outlined. The pathophysiological mechanisms of the phenomenon are briefly discussed. Intracranial hypotension is a potentially severe illness with specific treatments that are distinct from the treatment of most neurological diseases. Three cardinal features--postural headache, pachymeningitis, and descent of midline cerebral structures--should prompt the diagnosis.
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PMID:Intracranial hypotension presenting with severe encephalopathy. Case report. 972 24

Over the past 10 years, 10 cats with primary central nervous system infection by larvae of Cuterebra flies have been documented at Cornell University. Clinical abnormalities noted in all cats were progressive and most commonly consisted of depression (6/10), blindness (6/10), and behavior changes (2/10). Affected cats presented most commonly in July (2/10) and August (7/10); one cat was presented in September. The diverse histopathologic changes are unique to this aberrant migration and consist of a combination of five characteristic features: 1) parasitic track lesion (7/10), 2) superficial laminar cerebrocortical necrosis (10/10), 3) cerebral infarction (8/10), 4) subependymal rarefaction and astrogliosis with or without ependymal cell loss (7/10), and 5) subpial astrogliosis (7/10). Changes 2-5 occurred throughout the parenchyma unassociated with the track lesion or the parasite in the affected tissue. The larvae have been recovered most commonly in the region of the olfactory bulbs and peduncles, optic nerves, and cribriform plate, suggesting entry from the nasal cavity. Many of the changes noted are suggestive of a toxic factor elaborated by the parasite and borne within the cerebrospinal fluid, as well as vascular compromise as a component in those cats with brain infarction. Because of the prevalence of infarction associated with this syndrome and the lack of reported cases of such lesions in regions of the world devoid of the fly, we propose that aberrant cuterebral larval migration in the brain is the cause of feline ischemic encephalopathy.
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PMID:Cerebrospinal cuterebriasis in cats and its association with feline ischemic encephalopathy. 975 38

The ammonia and GABAergic neurotransmission hypotheses of the pathogenesis of hepatic encephalopathy (HE) have appeared to be unrelated and perhaps mutually exclusive. Observations in animal models of fulminant hepatic failure, that are consistent with increased GABAergic inhibitory neurotransmission contributing to the manifestations of HE, include: (i) abnormal visual evoked potential waveforms that resemble those induced by GABA(A)/benzodiazepine (BZ) receptor complex agonists; (ii) GABA(A)/BZ receptor complex antagonist-induced ameliorations of encephalopathy; (iii) increased resistance to drugs which decrease GABAergic tone; and (iv) hypersensitivity of CNS neurons to depression by GABA(A)/BZ receptor complex agonists. Mechanisms of increased GABAergic tone in HE may include the following: (i) increased brain concentrations of natural BZs; and (ii) increased GABA concentrations in synaptic clefts, possibly due to increased blood-brain-barrier permeability to GABA and a decrease in GABA(B) receptor density. Both neuroelectrophysiological and behavioral data indicate that ammonia concentrations in the range 0.75-2 mM induce increased excitatory neurotransmission. In contrast, recently, ammonia concentrations in the range 0.15-0.75 mM, i.e. concentrations that commonly occur in plasma in precoma HE, have been shown: (i) to increase GABA-induced chloride current in cultured neurons; and (ii) to enhance synergistically the binding of GABA(A)/BZ receptor agonists. In addition, increased ammonia concentrations enhance synthesis of neurosteroids in astrocytes, and some neurosteroids potently augment GABAergic neurotransmission. Thus, the modestly elevated concentrations of ammonia, that commonly occur in liver failure, may contribute to the manifestations of HE by enhancing GABAergic inhibitory neurotransmission. This concept appears to unify the ammonia and GABAergic neurotransmission hypotheses.
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PMID:Does ammonia contribute to increased GABA-ergic neurotransmission in liver failure? 1020 26

The objectives of this study were to determine in term infants: (1) the importance of maternal fever (maternal temperature > 38 degrees C) as a risk factor for neonatal depression and (2) the clinical course of infants admitted to the Neonatal Intensive Care Unit (NICU) born to mothers with fever. For 2 years, 59 (0.24%) of 25,000 term infants had a 5-minute Apgar score < or = 5 and 22 (0.08%) infants were administered chest compressions with or without epinephrine as part of cardiopulmonary resuscitation (CPR) in the delivery room. The perinatal event most commonly associated with a 5-minute Apgar score < or = 5 was maternal fever in 19 infants (32%), with meconium + fetal heart rate (FTHR) abnormalities in 15 (25%), and FTHR abnormalities only in 13 (22%), additional associations (n = 13). By stepwise linear regression analysis, a 5-minute Apgar < or = 5 was related only to the initial infant temperature (p = 0.009, r = 0.33). Maternal fever noted in six infants (27%) was also commonly associated with CPR, as was the presence of meconium + FTHR abnormalities in seven (32%), and FTHR abnormalities only in four (18%). One hundred thirteen (7.5%) of the approximately 1,500 term infants born to mothers with maternal fever were admitted to the NICU. In addition to fever, the labor was complicated by meconium (in 16 infants), meconium + FTHR abnormalities (in 19 infants), and FTHR abnormalities only (in 11 infants). Resuscitative interventions in the delivery room included oxygen only in 43 infants, bag and mask ventilation in 38, continuous positive airway pressure in 10, intubation in 16, and CPR in six infants. Forty-nine infants (43%) had an initial temperature > 38 degrees C including 13 (11%) with an initial temperature > 39 degrees C. Twelve (10%) infants remained intubated on admission and five required ventilator support > 24 hours. One blood culture was positive although all mothers were pretreated with antibiotics. One infant developed hypoxic ischemic encephalopathy including seizures. Maternal fever is the perinatal event most frequently associated with a 5-minute Apgar score < or = 5 and a common association with the need for CPR. Clinicians attending the delivery of a mother with fever should anticipate the potential for neonatal depression; such awareness should facilitate appropriate preparation before delivery and potentially reduce the need for more intensive resuscitation.
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PMID:Maternal fever and neonatal depression: preliminary observations. 1034 26

The efficacy of intravenous ceftriaxone, 2 g per day for 30 days, was evaluated in a case series of 18 consecutive patients who met strict criteria for Lyme encephalopathy. Months to years after classic manifestations of Lyme disease, the 18 patients presented with memory difficulty, minor depression, somnolence, or headache. Sixteen (89%) had abnormal memory scores; 16 (89%) had cerebrospinal fluid (CSF) abnormalities, and all 7 patients tested had frontotemporal perfusion defects on single photon emission computed tomographic (SPECT) imaging. Six months after treatment, memory scores in the 15 patients who completed the study according to protocol were significantly improved (P<.01). In the 10 patients who had follow-up CSF analyses, total protein levels were significantly lower (P<.05). In the 7 patients who had SPECT imaging, posttreatment perfusion was significantly better (P<.01). Twelve to 24 months after treatment, all 18 patients rated themselves as back to normal or improved. We conclude that Lyme encephalopathy can be treated successfully with ceftriaxone.
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PMID:Successful treatment of Lyme encephalopathy with intravenous ceftriaxone. 1039 52

Central nervous system infections in children and adolescents involve a wide spectrum of illnesses, ranging from acute self-limited diseases, such as enteroviral meningitis, to severe diffuse or focal infections (i.e., arboviral encephalitis) resulting in devastating neurologic sequelae. All the clinical manifestations of CNS infections occur to some degree secondary to toxic mediators such as cytokines. These factors are neurotoxic and produce clinical manifestations such as encephalopathy, motor abnormalities, and seizures. Many of these diseases also produce radiculoneuropathies and vasculopathies (stroke). As a result, chronic neurologic conditions may result and are frequently associated with psychiatric disturbances and situational depression.
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PMID:Neurobehavioral manifestations and sequelae of HIV and other infections. 1055 8

Ifosfamide is an alkylating agent used in the treatment of a variety of solid tumours. Ten to 15% of patients treated with ifosfamide develop an encephalopathy. Methylene blue (MB) may be used in the treatment of this encephalopathy. The purpose of this study was to evaluate the neuroprotective effect of MB in these patients and to review the literature. Between 1993 and 1997, 52 patients (age 16-77 years) with solid tumours were treated with ifosfamide in dosages ranging from 3 to 5 g m(-2) q3w when given in combination schedules and up to 12 g m(-2) q4w when given as a single agent. Twelve patients developed central nervous system (CNS) depression, defined as National Cancer Institute Common Toxicity Criteria (NCI-CTC) neurocortical toxicity grade 2 or higher. Eight were treated with MB at a dose of 6 x 50 mg day(-1) intravenously (i.v.). Four recovered fully within 24 h, two recovered partially after 24 h and completely after 48 h while two recovered only after 72 h. Four patients did not receive MB and all recovered only after 48 h. Three patients received prophylaxis with MB at a dose of 4 x 50 mg day(-1) i.v. for the subsequent chemotherapy cycles. Two developed milder encephalopathy; one had no CNS depression at all. We conclude that MB is an effective treatment for ifosfamide-induced encephalopathy. Our findings suggest that it may also be used as a prophylactic agent.
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PMID:Methylene blue in the treatment and prevention of ifosfamide-induced encephalopathy: report of 12 cases and a review of the literature. 1064 79

We report the unusual features of a female patient who had MELAS-specific A3243G mutation in mitochondrial DNA (mtDNA) and diabetes mellitus (DM). The patient showed mitochondrial myopathy, encephalopathy, lactic acidosis, and deafness but lacked the stroke-like episode. Acute hyperglycemia was noted after one attack of status epilepticus. Molecular genetic analysis demonstrated a heteroplasmic A3243G point mutation in the mtDNAs of muscle, blood cells and hair follicles. Glucagon stimulation test exhibited marked depression of pancreatic beta-cell function. However, in a further study neither this mutation, nor MELAS syndrome or DM, was found in all of her maternal relatives. A series of follow-up studies for beta-cell function also showed gradual improvement. The pedigree study led us to believe that this A3243G mutation arose from the germ line cells or occurred later in somatic tissues of the patient. We also suggest that the A3243G mutation of mtDNA may elicit the pathogenesis of a subtype of DM. Nevertheless, environmental stress may be another important factor for provocation of the disease.
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PMID:Absence of maternal A3243G mtDNA mutation and reversible hyperglycemia in a patient with MELAS syndrome. 1066 Jan 56


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