Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0018681 (headache)
 56,091 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The case histories of two patients with acute lymphocytic leukemia, who developed central nervous system complication during combined chemotherapy are described. The neurological picture could be characterized by symptoms of headache, mental deterioration, hemiparesis and seizures. Following L-asparaginase administration one patient had intracranial thrombosis with focal seizures and hemiparesis associated with clotting abnormalities, including severe hypofibrinogenemia and decreased antithrombin III activity. In the other patient, it was after intrathecal administration of Methotrexate when mental deterioration associated with the symptoms of progressive leukoencephalopathy occurred. It arises the possibility that with increasing complexity of combined chemotherapy the occurrence rate of neurological complications will also increase.
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PMID:[Neurologic complications during chemotherapy of children with acute lymphoid leukemia]. 157 51

A 14-year-old boy, suffering from acute lymphoblastic leukemia with meningeal involvement, was treated with intraventricular methotrexate and cytosine arabinoside, administered via an Ommaya reservoir (OR). Three months later, right occipital headache, vomiting, and lethargy appeared. Cerebrospinal fluid specimens showed increased proteins and a right frontal slow-wave focus was evident on the EEG recording. The computed tomography scan revealed white matter hypodensity within the right frontal and rolandic regions. After injection of medium contrast, an abscesslike hyperdensity appeared, surrounding both a well-placed cannula tip and the right frontal horn of the lateral ventricle. Brain swelling and shift signs were also evident. Nine cases of focal methotrexate leukoencephalopathy have been previously reported, and in six of these there was a misplaced OR cannula tip. The focal methotrexate leukoencephalopathy seems to be related to the neurotoxicity of the drugs administered, and may also exist with a well-placed OR cannula tip. Immediate removal of the catheter may be associated with a benign evolution.
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PMID:Transient focal leukoencephalopathy following intraventricular methotrexate and cytarabine. A complication of the Ommaya reservoir: case report and review of the literature. 220 Jun 10

A case of long-term survival of a female patient with complicated diffuse metastatic leptomeningeal carcinomatosis (DMLC) secondary to lung cancer is reported. A 36-year-old woman, hospitalized with a chief complaint of headache and unproductive cough, was diagnosed as having primary lung adenocarcinoma (T4N1M1 oss) and was given systemic chemotherapy. Although progressive deterioration of her headache continued, repeated neurological examination, cerebrospinal fluid (CSF) examination, and cranial CT scans failed to show evidence of metastasis to the central nervous system, and the only finding suggesting CNS involvement was an elevated CEA level in CSF. Later in the course of her treatment, the patient suddenly lost her vision and subsequently consciousness due to acute increased intracranial pressure, and emergency ventricular drainage was performed for therapeutic and diagnostic purposes. Malignant cells were found in CSF obtained from a ventricular drainage and she was treated successfully by systemic and intrathecal chemotherapeutic agents. She was discharged after a ventriculoperitoneal shunt operation for hydrocephalus; a double-dome reservoir was used for continuous intrathecal administration of the anticancer drugs, and a shunt filter was located in the tube to prevent the dissemination of cancer cells. In addition to methotrexate and cytosine arabinoside, ACNU and interleukin-2 were administered intrathecally without serious adverse effects, but no apparent therapeutic effects were noted either. She survived over 2 years after DMLC was first diagnosed. At autopsy DMLC secondary to lung adenocarcinoma was confirmed, but no evidence of leukoencephalopathy due to aggressive intrathecal chemotherapy was found. Current therapy for patients with DMLC and its clinical problems are discussed in relation to our experience in this case.
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PMID:[A case of long-term survival of a patient with complicated diffuse metastatic leptomeningeal carcinomatosis secondary to lung adenocarcinoma]. 224 65

Seventy to eighty percent of HIV-infected patients exhibit neurological disorders at an advanced stage of the disease. In almost 90% of cases anatomical examination of brains shows histological lesions. Even when often reversible neurological disorders occur during the HIV primary infection, most of the manifestations of central nervous system (CNS) damage remains the prerogative of severe immunodepression. The principal CNS lesions associated with HIV infection are presented here with the clinical and biological elements that lead to the diagnosis. Cerebral toxoplasmosis holds a privileged place in these manifestations since it responds to an efficient curative and prophylactic treatment with a well-codified medical care based on the test treatment. Biological data, therefore, only have a contributing value. HIV encephalopathy is frequent, but the dementia syndrome is less frequent than the finding of associated imaging and pathological anatomy: atrophy and lesions of the white matter. Thus, the dementia complex is an elimination diagnosis. Cryptococcosis must be systematically considered, not only in patients with meningeal symptoms and headaches, but also with those with isolated fever. The demonstration of cryptococcus and cryptococcic antigen in the CSF has an almost absolute diagnostic value; imaging plays a very small diagnostic role, looking for an exceptional cryptococcoma. Multifocal progressive leukoencephalopathy benefits from the accuracy of MRI, and the diagnosis is usually based on clinical data, MRI and evidence of the virus in the CSF by PCR, even though the only mean of obtaining full proof is, in theory, stereotaxic biopsy. Primary cerebral lymphoma is the diagnostic alternative to toxoplasmosis.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Clinical and paraclinical diagnosis of AIDS neurologic lesions]. 747 28

This paper reports a Swiss family affected by a cerebral autosomal dominant arteriopathy with subcortical infarcts and leukoencephalopathy (CADASIL) linked to chromosome 19q12. In three generations several members of this family had recurrent stroke-like episodes and, some developed subcortical dementia, migraine-like headaches, and depression. The clinically affected family members had multiple subcortical infarcts and diffuse leukoencephalopathy on MRI. Necropsy of one patient showed a distinctive non-amyloid and non-atherosclerotic angiopathy of small cerebral and leptomeningeal arteries with concentric depositions of a basophilic granular material replacing the smooth muscle cells of the media. Linkage analysis with five chromosome 19 markers spanning the estimated CADASIL interval showed the absence of any recombinant and positive Lod scores, highly suggestive of linkage of this condition to the CADASIL locus. CADASIL might be an underestimated cause of familial stroke and should be considered in the differential diagnosis of hereditary stroke.
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PMID:Cerebral autosomal dominant arteriopathy with subcortical infarcts and leukoencephalopathy: a clinicopathological and genetic study of a Swiss family. 762 27

A 61-year-old woman was treated with cisplatin and etoposide for ovarian carcinoma. After the second course of chemotherapy she developed acute encephalopathy which manifested itself as headache, fever, a partial seizure, confusion, and mild right hemiparesis, although no evidence of a central nervous system infection was found. Ten days after the onset of neurological symptoms, she experienced a sudden loss of vision in both eyes. Neurological findings were compatible with cortical blindness. Neurological symptoms subsided and visual acuity completely returned over the next months. The total cumulative dose of cisplatin was 325 mg/m2. She died of aspiration pneumonia on the 43rd day. Postmortem examination revealed severe nerve cell loss, gliosis and spongy changes in the bilateral occipital cortex including visual field, and slight to moderate demyelination in the subcortical white matter of the occipital cortex, Goll's tract, and dorsal root ganglia. As far as we know this encephalopathy is the second report in which the neuropathological changes associated with cisplatin therapy have been demonstrated by autopsy findings. The first was a case report of leukoencephalopathy, which differed significantly from our case in the primary lesions of the brain. We measured the platinum level in several parts of the cerebrum and cerebellum, optic nerve, spinal cord, and cauda equina by using an atomic absorption spectrophotometric technique. Platinum was detected in the bilateral occipital cortex, spinal cord, and cauda equina. These results were consistent with the distribution of pathological lesions. The mechanism of cisplatin-induced focal encephalopathy remains speculative.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Clinicopathological report of cisplatin encephalopathy]. 778 Dec 18

A 23-year-old black female presented with general malaise, headache, high white cell count (136 x 10(9)/L), thrombocytopenia and nephrotic syndrome. She proved to have large granular lymphoproliferative disease with a natural killer cell phenotype and without a clonal rearrangement of the T-cell receptor genes. Renal biopsy demonstrated focal segmental glomerulosclerosis (FSGS). She developed a monophasic neurological illness, and rapidly became comatose six days after the initiation of high dose prednisone therapy. Computerized tomography of the brain showed marked hypodensity of the subcortical white matter. She regained consciousness subsequently, but died six months after her initial presentation with uncontrolled lymphocytosis and renal failure. Autopsy revealed FSGS with glomerular collapse and microcystic dilatation of the renal tubules, and there was perivascular demyelination in the subcortical white matter of the brain. We speculate that lymphokines released by the natural killer cells may have played an important role in the pathogenesis of both the nephrotic syndrome and leukoencephalopathy.
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PMID:Large granular lymphoproliferative disease associated with nephrotic syndrome, renal failure and leukoencephalopathy. 822 Jan 46

A boy presented with hypertension, seizures, lethargy, headache, and occipital blindness. He improved with antihypertensive therapy. Other reported children with a similar distinctive clinical condition are compared with adults with a syndrome termed reversible posterior leukoencephalopathy. Because both gray and white matter are involved, we suggest that the name be changed to occipital-parietal encephalopathy syndrome.
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PMID:Occipital-parietal encephalopathy: a new name for an old syndrome. 930 87

Human recombinant erythropoietin is used to treat chronic anemia in patients with end-stage renal failure. Erythropoietin causes hypertension, and hypertensive encephalopathy has been associated with its use. We describe six dialysis-dependent, chronic renal failure patients who developed hypertension, headache, and seizures while on erythropoietin. Four of the six patients had posterior white matter changes on neuroimaging. The encephalopathy was managed by prompt antihypertensive and anticonvulsant treatment and by discontinuation of erythropoietin. Hypertensive posterior leukoencephalopathy is associated with erythropoietin use.
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PMID:Erythropoietin-associated hypertensive posterior leukoencephalopathy. 971 75

Organ transplantation has become a practical and effective option for patients with acute and/or chronic irreversible organ disease. However, solid organ transplantation is associated with many different complications which depend upon the specific surgical procedure and/or confounding medical problems (e.g. rejection, infection, adverse effect of immunosuppressive agents) experienced by a given patient. Tacrolimus and cyclosporin A are immunosuppressive drugs used to prevent rejection following allogeneic solid organ transplantation. Adverse events are common with both drugs and include long-term organ dysfunction, opportunistic infections, haematopoietic alterations, nephrotoxicity and neurotoxicity. Neurological complications, both central and peripheral, occur in 10-42% of transplant recipients using either of these two immunosuppressive agents. Two cases of reversible posterior leukoencephalopathy manifested by headache, nausea and seizures associated with the use of immunosuppressive drugs following liver transplantation are reported.
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PMID:Immunosuppressive drug-induced leukoencephalopathy in patients with liver transplant. 961 93


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