1/33. Central anticholinergic syndrome in anesthetic practice.Anticholinergic agents may lead to a syndrome described by Longo as the Central anticholinergic syndrome (CAS). patients with this syndrome exhibit one or more of the following: though impairement, disturbance of recent memory, hallucinations, ataxia, excitement, drowsiness of coma. We have reviewed our use of anticholinergics and tried to correlate it with the occurrence of the above symptomatology and have treated 200 cases in which the CAS was diagnosed with physostigmine salicylate (0.04 mg/kg). We also successfully treated 2 cases of apparently central anticholinergic hyperpyrexia in the same way. We would suggest that physostigmine be included in the armamentarium of every anesthetist to combat anticholinergic poisoning by the wide range of presently used anticholinergic drugs. (Act anaesth. belg., 1976, 27, 45-60).- - - - - - - - - - ranking = 1keywords = coma (Clic here for more details about this article) |
2/33. Severe neurological complications of ulcerative colitis.A 37 year old man presented with a 15 year history of ulcerative colitis. On examination he had weakness of the right arm, slurred speech and progressive confusion, followed by a rapid deterioration of consciousness and motor functions resulting in coma, tetraparesis and bilateral Babinski responses. magnetic resonance imaging of the brain and spinal cord revealed multiple hyper- and hypointense white matter lesions. Clinical symptoms, history and neuroradiological findings led to the diagnosis of an ulcerative colitis-associated CNS disorder. An autoimmune vasculitic process may have played an important pathophysiological role, considering the vasculitic changes observed by skin biopsy as well as the rapid clinical improvement following immunosuppressive therapy with corticosteroids and azathioprine. During a follow up period of more than one year we observed continuous and complete recovery of neurologic symptoms.- - - - - - - - - - ranking = 1keywords = coma (Clic here for more details about this article) |
3/33. Parainfectious encephalomyeloradiculitis associated with herpes simplex virus 1 dna in cerebrospinal fluid.We describe a patient with acute encephalomyeloradiculitis associated with herpes simplex virus 1 (HSV-1) dna in the cerebrospinal fluid (CSF), and we also review 4 similar cases previously reported from japan. A 59-year-old man presented with acute encephalitis and urinary retention. Initially, coma and CSF pleocytosis improved with acyclovir treatment, but brain stem encephalitis, transverse myelitis, and lumbosacral polyradiculitis subsequently occurred. These conditions responded to corticosteroid therapy and immunoadsorption plasmapheresis. polymerase chain reaction detected HSV-1 dna in the CSF during acute encephalitis but not thereafter. Serial magnetic resonance imaging revealed transient lesions in the thalamus and basal ganglia on both sides of the brain and in the pons, spinal cord, and cauda equina. Acute encephalomyeloradiculitis is a unique neurological syndrome that may be caused by HSV-1 infection of the central nervous system.- - - - - - - - - - ranking = 1keywords = coma (Clic here for more details about this article) |
4/33. anticholinergic syndrome after anesthesia: a case report and review.anticholinergic syndrome may present with a wide variety of signs and symptoms. Central manifestations range from excitatory symptoms including delirium and agitation to central nervous system depression, stupor and coma. Anticholinergic syndrome was once a common phenomenon after general anesthesia because of the frequent administration of the anticholinergic agents atropine and scopolamine. Now that these agents are rarely administered, anesthesia-related anticholinergic syndrome is currently infrequently reported. Still, many prescription and over the counter medications as well as many anesthetic agents possess anticholinergic activity, and this diagnosis should be considered in patients with altered mental status following general anesthesia. We report a case of prolonged somnolence following general anesthesia for an MRI. A rapid improvement of mental status with physostigmine confirmed the diagnosis of anticholinergic syndrome. This case is unique in that anticholinergic syndrome-related respiratory depression was promptly reversed with physostigmine.- - - - - - - - - - ranking = 1keywords = coma (Clic here for more details about this article) |
5/33. Inadvertent intrathecal injection of daunorubicin with fatal outcome.We report the first known case of daunorubicin administered directly into the human central nervous system. A 3 1/2-year-old female with pneumonia and otitis media was diagnosed with acute lymphoblastic leukemia and was admitted for antibiotics and chemotherapy. On the first day she inadvertently received a 17 mg intrathecal (IT) injection of daunorubicin. When the error was recognized about 1 hour later, her cerebrospinal fluid (CSF) was exchanged with sterile saline by barbotage, IT hydrocortisone was given, a subarachnoid catheter was inserted, and the CSF was allowed to drain for 36 hours. Only 5.6 mg (33%) of the dose was recovered from CSF, 2.7 mg as daunorubicin and 2.9 mg as the metabolite, daunorubicinol. Initially she was asymptomatic and induction therapy continued with vincristine, 1-asparaginase, prednisone, and IT methotrexate. One week after the daunorubicin injection she developed headache and irritability; CSF protein was 3.2 gm/dl. On the 12th day, she developed fungal sepsis and worsening pneumonia. On the 15th day, she became comatose with a flacid paraparesis, areflexia, and an ascending progressive bulbar palsy. A series of computerized tomography scans over 6 weeks showed increasing diffuse cerebral atrophy. Nerve conduction velocity studies were consistent with an axonal neuropathy. Despite her multiple concurrent medical problems, the timing and characteristics of neurologic damage suggest that IT daunorubicin caused progressive destruction of the nervous system.- - - - - - - - - - ranking = 1keywords = coma (Clic here for more details about this article) |
6/33. 5-fluorouracil can cross brain-blood barrier and cause encephalopathy: should we expect the same from capecitabine? A case report on capecitabine-induced central neurotoxicity progressing to coma.PURPOSE: Capecitabine is a relatively new oral fluoropyrimidine currently licensed for the treatment of colorectal and breast cancer. RESULTS: It has the advantage of oral administration with good tolerability and comparable activity to intravenous 5-fluorouracil. Central neurotoxicity has been described in 5-fluorouracil-treated patients but there is little data regarding capecitabine. We report here a case of reversible capecitabine-induced encephalopathy progressing to coma. DISCUSSION: literature on fluoropyrimidine-related neurotoxicity will also be reviewed and possible mechanisms of the drug or its metabolites crossing the blood-brain barrier will be discussed.- - - - - - - - - - ranking = 5keywords = coma (Clic here for more details about this article) |
7/33. central nervous system magnesium deficiency.The central nervous system concentration of magnesium (Mg ) appears to have a critical level below which neurologic dysfunction occurs. Observations presented suggest that the interchange of the Mg ion between the cerebrospinal fluid, extracellular fluid, and bone is more rapid and dynamic than is usually believed. This is especially so when the hypertrophied parathyroid gland is associated with significant skeletal depletion of Mg as judged by history rather than serum level. Magnesium, much like calcium, has a large presence in bone and has a negative feedback relationship with the parathyroid gland. A decline in central nervous system Mg may occur when the skeletal buffer system orchestrated largely by the parathyroid glands is activated by an increase in serum calcium. Observations in veterinary medicine and obstetrics suggest that the transfer of Mg from the extracellular fluid into bone during mineralization processes may be extensive. If the inhibition of the hypertrophied parathyroid gland is prolonged and the skeletal depletion of Mg extreme, serious neurologic symptoms, including seizures, coma, and death, may occur. noise, excitement, and bodily contact appear to precipitate neurologic symptoms in Mg ( )-deficient human subjects as it has been documented to occur in Mg ( )-deficient experimental animals. The similarity of the acute central nervous system demyelinating syndromes with reactive central nervous system Mg deficiency is reviewed.- - - - - - - - - - ranking = 1keywords = coma (Clic here for more details about this article) |
8/33. Granulocytic sarcoma of the central nervous system: inital presentation of leukemia.Granulocytic sarcoma as the presenting feature of leukemia is rare. Although it has been reported in various sites such as the retrobulbar area, mastoid region, iliac bone, and breast, this appears to be the first recorded case presenting as an intracranial tumor.- - - - - - - - - - ranking = 5keywords = coma (Clic here for more details about this article) |
9/33. Does central nervous system toxicity occur in transplant patients with hypocholesterolemia receiving cyclosporine?A syndrome of severe central nervous system toxicity (confusion, cortical blindness, quadriplegia, seizures, and coma) associated with cyclosporine therapy and a low serum cholesterol level in patients with liver transplants has been described. We present a case history of a patient who demonstrated several similar features after heart-lung transplantation. Possible cyclosporine neurotoxicity should be considered in any patients with hypocholesterolemia receiving this drug.- - - - - - - - - - ranking = 1keywords = coma (Clic here for more details about this article) |
10/33. chromosomes and causation of human cancer and leukemia. XXXIV. A case of "hypereosinophilic syndrome" with unusual cytogenetic findings in a chloroma, terminating in blastic transformation and CNS leukemia.A 47-year-old white male developed massive hepatosplenomegaly, a pleural effusion, leucocytosis, and a left parasternal mass following a relatively symptom-free persistent hypereosinophilia for about 5 years. Bone marrow aspiration and biopsy and peripheral blood differential showed eosinophilia and a shift to the left with immature cells. A high serum B12 vitamin level and low LAP activity were found. biopsy of the soft tissue mass revealed a granulocytic sarcoma (chloroma) with a hyperdiploid karyotype (49,XY, 10, 15, 19,3q-), whereas the bone marrow cells had a normal male karyotype. The patient responded temporarily to chemotherapy but eventually developed CNS leukemia and went on to terminate in a frank blastic phase. This case illustrates hypereosinophilia and a myeloproliferative syndrome characterized by a somewhat indolent chronic course evolving into "eosinophilic leukemia" and granulocytic sarcoma, CNS involvement by leukemic cells and, finally, blastic transformation. It is possible that this case represents a variant of Ph1-negative CML to which the term "chronic eosinophilic leukemia" could be justifiably applied.- - - - - - - - - - ranking = 2keywords = coma (Clic here for more details about this article) |
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