Increased cerebrospinal fluid levels of cytokines monocyte chemoattractant protein-1 (MCP-1) and macrophage inflammatory protein-1ß (MIP-1ß) in patients with amyotrophic lateral sclerosis. / Incremento de las citoquinas proteína quimiotáctica de monocitos-1 (MCP-1) y proteína inflamatoria macrofágica-1ß (MIP-1ß) en líquido cefalorraquídeo de pacientes con esclerosis lateral amiotrófica.

INTRODUCTION: Neuroinflammation has recently been described in amyotrophic lateral sclerosis (ALS). However, the precise role of such proinflammatory cytokines as monocyte chemoattractant protein-1 (MCP-1) and macrophage inflammatory protein-1ß (MIP-1ß) in ALS has not yet been determined. In this study, we determined cerebrospinal fluid (CSF) MCP-1 and MIP-1ß levels and assessed their association with the duration and severity of ALS. METHODS: Concentrations of MCP-1 and MIP-1ß were determined in the CSF of 77 patients diagnosed with ALS and 13 controls. Cytokine levels were analysed in relation to ALS duration (<12months vs. >12months) and severity (<30points vs. >30points on the ALS Functional Rating Scale administered at hospital admission). RESULTS: Higher CSF MIP-1ß (10.68pg/mL vs. 4.69pg/mL, P<.0001) and MCP-1 (234.89pg/mL vs. 160.95pg/mL, P=.011) levels were found in the 77 patients with ALS compared to controls. There were no differences in levels of either cytokine in relation to disease duration or severity. However, we did observe a significant positive correlation between MIP-1ß and MCP-1 in patients with ALS. CONCLUSIONS: The increase in MIP-1ß and MCP-1 levels suggests that these cytokines may have a synergistic effect on ALS pathogenesis. However, in our cohort, no association was found with either the duration or the clinical severity of the disease.

Short communication: Graph for calculating maximum local analgesic dose in millilitres for the paediatric population.

AIM: Determination of the maximum local analgesic dosage in millilitres can be confusing. This article presents a new graph that easily allows the dental practitioner to determine a child's maximum local analgesic dosage in millilitres based on their weight. BACKGROUND: Local analgesia is used daily in dentistry to manage pain, and different kinds of agents are available in the market that may be selected depending on the strength and duration of analgesia required. Each analgesic agent has a maximum recommended dose, and it is very important to calculate that dose, especially in children, to avoid the risk of toxicity that could lead to death. Currently a series of calculations are used to calculate the maximum recommended dose for local analgesic agents that could be taxing. This paper presents a newly-developed graph that makes it easier for dental practitioners to quickly identify the maximum recommended dose of the different local analgesic agents used in dentistry based on a patient's weight. CONCLUSION: Dentists can utilize this graph to obtain the maximum local analgesic dose in millilitres based on the child's weight. This will save time and encourage dentists to routinely identify the maximum allowed dose and most importantly, decrease or eliminate the risks of toxicity and overdose especially when treating small children.

Clinical diagnosis in Karwinskia humboldtiana polyneuropathy.

Intoxication by Karwinskia humboldtiana presents a neurological picture similar to that for Guillain-Barré syndrome or other polyradiculoneuropathies. Clinical diagnosis in poisoned humans may be difficult if no evidence of previous fruit ingestion is available. We present our experience in the clinical diagnosis of Karwinskia humboldtiana polyneuropathy, as confirmed by toxin detection in blood. We designed an open trial at the Pediatric Neurology service and included all cases with acute ascending paralysis that were admitted to our hospital in the last two years. In all cases, we performed hematological, immunological and biochemical profiles, CSF analysis including immunological studies, oligoclonal bands and myelin basic protein determinations. Electrodiagnostic studies were performed, including motor conduction velocities, distal latencies, F-wave latency and compound muscle action potential (CAMP) amplitude. The presence of Karwinskia humboldtiana toxins in blood were determined by thin layer chromatography. In six cases, T-514 Karwinskia humboldtiana toxin was detected. These cases had a symmetric motor polyneuropathy with the absence of tendon reflexes and no sensory signs or cranial nerve involvement. Only one patient required assisted ventilation due to bulbar paralysis. In two of these cases, a sural nerve biopsy revealed a segmental demyelination with swelling and phagocytic chambers in Schwann cells and without lymphocytic infiltration. All six cases survived, with complete recovery in five. We conclude that this intoxication is common in Mexico. The availability of toxin detection in blood samples allows the clinician to establish an accurate diagnosis and should be included in the study of children with polyradiculoneuropathy, especially in countries where this poisonous plant grows.

Rhinocerebral and systemic mucormycosis. Clinical experience with 36 cases.

We analysed retrospectively our clinical experience with 36 cases of mucormycosis. They were seen during the last 15 years. The diagnosis suspected on clinical grounds, was confirmed in 31 cases by finding the hyphae in hematoxylin-eosin stained material obtained from aspirated or tissue biopsy or by isolation of the fungus in culture. Rhinocerebral mucormycosis was diagnosed in 22 patients. Diabetes was the underlying disorder in 20 cases, kidney failure in one and myelodysplastic syndrome in one. Nine had stable and 11 unstable diabetes (ketoacidosis in 10 and hyperosmolar coma in 1). The earliest sign was facial edema, followed by proptosis, chemosis and extraocular muscle paresis. They were treated by extensive surgical debridement, insulin and antifungal drugs with 69% of survival rate. The disseminated mucormycosis was diagnosed at the autopsy in 5 cases, acute leukemia was the underlying disease in 2 of them. Pulmonary mucormycosis was diagnosed in 2 cases, cutaneous form in 2, sinuorbital form in 4 and brain abscess in one patient. Eight of these 9 cases survived after therapy. We emphasize the importance of an early diagnosis. This can only be made in the presence of a typical clinical setting confirmed by finding the hyphae in tissue or culture. Antifungal drugs along with treatment of the underlying disorder and aggressive surgical debridement must follow.

Medical and surgical treatment in neurocysticercosis a magnetic resonance study of 161 cases.

In a prospective non-controlled study we have treated 161 consecutive cases of Active Neurocysticercosis (NCC) diagnosed by Magnetic Resonance (MR). Active NCC was classified in: (1) brain parenchymal cysts (85 cases); (2) ventricular cysts (24 cases); (3) subarachnoid cysts (46 cases); and (4) cysticercus racemose (6 cases). All patients had MR follow up 1 month after treatment. Twenty five patients had MR with gadopentetate dimeglumine (Gd) contrast enhancement. Cine MR was performed in one patient. Medical treatment with albendazole (ABZ) or Praziquantel (PZQ) was applied in 136 cases. Drug efficacy, assessed by disappearance of the lesion on MR, was 92.5% with ABZ and 60% with PZQ. Thirty patients were treated by surgery. Five patients of group I were treated surgically due either to refractory seizures or persistent abnormalities on MR. Ventricular cysts were removed in 20 cases; 4 cases with cysticercus racemose and one with subarachnoid spinal cyst were also treated by surgery. Two patients with 4th ventricle cysts received ABZ and ventricular shunt only. Two cases with intraventricular cysts (lateral ventricles) and two with racemose cysts were successfully treated with ABZ. The Gd infusion showed enhancement in cysts with adjacent inflammatory reaction or edema and in cases with meningeal inflammation. Cine MR was useful in the differential diagnosis with congenital arachnoid cyst. We conclude that (1) MR is sensitive in the diagnosis of active NCC and may be useful in evaluating degenerative changes in the parasite; (2) ABZ is highly effective in the treatment of parenchymal and subarachnoidal NCC; (3) Parenchymal lesions which remain with abnormal appearance on MR (Degenerative cysticerci or gliosis) and refractory seizures should be treated by surgery; (4) Cysticercus racemose without intracranial hypertension may be treated with ABZ; (5) Ventricular cysts are treated by surgical removal, however, ABZ and ventricular peritoneal shunt may also be an alternative approach.

Cost of stroke in Mexico.

We report the estimated costs of stroke management in Mexico. The cost of stroke in our country has not been formerly described previously. The costs were estimated from population-based studies: the national survey on stroke and those performed by the Health Mexican Foundation. Other sources were the administration of private hospitals and official statistics obtained from the National Institute of Informatic, Statistic and Geography. Of 89 million Mexicans, 6.1% are older than 60 years. Based on the national stroke survey, it was calculated that 32,000 people suffer from stroke each year. Their mean age is 63 years. The estimated cost of acute stroke care in 1994 was $7,700 (U.S. dollars) per patient in private hospitals and $6,600 in institutions of the health sector. The major portion of the costs were spent in diagnostic procedures (40%). Physician costs ranged from 12% to 19%. The average in-hospital stay was 9 days with 18% in hospital mortality rate. About 20% of the total population are not covered by health care institutions. The cost of stroke care in Mexico is lower than in industrialized countries because of a shorter hospital stay and lower personnel wages. Indirect costs for chronic care are unknown in our country. The number of people older than 60 years will increase in the next century; hence, the number of persons with stroke will rise.

[Reye's syndrome in an adult. Review of pathogenic mechanisms]. / Síndrome de Reye en un adulto. Revisión de los mecanismos patogénicos.

Reye's syndrome is considered a disease of the pediatric age. It is characterized by a prodrome of viral illness followed by vomiting and encephalopathy with associated hepatic dysfunction. This syndrome is potentially life-threatening with high morbidity and mortality rates. There are 27 other cases of adult onset Reye's syndrome reported in the literature. We describe a 18-year-old woman who developed varicella and four days later started with vomiting, delirium and in the following day she became comatose. Laboratory tests of liver function and pathology of a liver biopsy proved the diagnosis. The patient survived. A review of the proposed pathogenic mechanisms are presented. Our patient represents case the number 28 in world literature and the first in the mexican literature.

Ischemic stroke due to deficiency of coagulation inhibitors. Report of 10 young adults.

BACKGROUND AND PURPOSE: Deficiencies in coagulant inhibitors protein C, protein S, and antithrombin III increase the risk of venous thrombosis. We describe 10 young adults with cerebral arterial thrombosis due to deficiencies in these factors. METHODS: Sixty patients younger than 45 years were hospitalized because of acute ischemic stroke diagnosed through computed tomography or magnetic resonance imaging. Cerebral angiography was performed in 54 cases. Hematologic and coagulation profiles, autoantibody screen, syphilis serology, and lupus anticoagulant were analyzed in all patients. Among the total cases, Holter monitoring was performed in 13 patients, echocardiography in 20, and cerebrospinal fluid studies for cysticercosis and tuberculosis in two. The quantitative analysis of protein C, protein S (by Laurell rocket immunoelectrophoresis), and antithrombin III (by radial immunodiffusion) was performed on admission and 3 months after stroke in all patients and in relatives of six patients. RESULTS: In 10 cases (17%) the stroke was attributed to deficiency of coagulation inhibitors: three men had protein C deficiency, two women had protein S deficiency, and five had antithrombin III deficiency (three men and two women). The cerebral infarction involved the carotid territory in these 10 patients. None had previous thromboembolic disease. Eight patients showed a complete recovery. An acquired disorder was presumed in one protein S-deficient and in two antithrombin III-deficient patients; the remainder were considered heterozygous. CONCLUSIONS: The cerebral vasculature may be primarily involved in the deficiency of these natural anticoagulants. Young adults seem to be the most often affected. A knowledge of these new clotting defects will enable the clinician to improve the prevention and treatment of this devastating neurological disease.

[9 cases of encephalitis in an epidemic outbreak of exanthematous diseases]. / Nueve casos de encefalitis en un brote epidémico de enfermedades exantemáticas.

We report here nine cases of encephalitis secondary to exanthematous diseases diagnosed from March to June 1990 at the University Hospital in Monterrey, Mexico. Two of the cases were secondary to measles, three to rubella, and four to varicella. One patient with varicella died, and the histopathological study showed findings compatible with viral encephalitis. The sex distribution was four males and five females with ages ranging from two to fourteen years. The most common clinical manifestations were hemiparesia, intracranial hypertension, meningism and altered consciousness. The CSF examination showed lymphocytic pleocytosis (mean = 295 cells), increased protein levels (mean = 118 mg/dL) and a normal glucose value in eight cases. These findings and the presence of an exanthematous disease suggested viral invasion of the CNS. Magnetic resonance imaging showed high intensity signal areas mainly in the frontal and temporal lobes. In this paper we compare the relative incidence of encephalitis secondary to exanthematous diseases in our geographical area during the last four years.

[Epilepsy and thyrotoxicosis in a 4-year-old boy]. / Epilepsia y tirotoxicosis en un niño de cuatro años.

Hyperthyroidism in childhood has a relative incidence of 5%. The presence of epilepsy secondary to thyrotoxicosis is very unusual. We report the case of a four-year old boy with thyrotoxicosis due to Graves' disease. This patient developed a generalized tonic-clonic seizure followed by left sided partial motor status epilepticus. The EEG was markedly abnormal. The EEG was normal after five months of the ablative therapy. At the present time the patient is seizure-free without any antiepileptic medication and receiving replacement therapy with thyroxin due to post-ablation hypothyroidism. We conclude that this is the first reported case with this association in our country. We discuss the possible pathophysiological mechanism involved in the development of seizures in this patient.

[Thallium poisoning. Experience with 50 patients]. / Intoxicación por talio. Experiencia con 50 pacientes.

We have studied fifty cases of thallium intoxication during the past nine years. Twenty-eight occurred in women and twenty-two in men. One of the patients was a new born whose mother had this type of intoxication during her third trimester of pregnancy. The ages varied from one day to 84 years and in all cases the source of thallium was ingestion of rat poison, except for the baby who received it across the placenta and an other patient whose source was transdermal. Twenty-three of the cases of intoxication were accidental, twenty-one were suicidal attempts and five were homicidal. One case did not know the source of intoxication. Thallium levels were measured in the urine of all the patients, some were measured in blood, as well as cerebrospinal fluid. The main clinical manifestation was a mixed type of severe peripheral neuropathy, with abdominal pain, nausea, vomiting and alopecia and some cases had psychiatric manifestations. Electrophysiological studies and nerve biopsy examined with electron microscopy in three patients. Magnetic nuclear resonance, computerized axial tomography of the abdomen and cranium were performed in two patients. There was only one death and the rest of the patients recovered almost completely. Pathophysiology and pharmacological management of this type of neurointoxication are revised.

[Diagnosis of thrombosis of cavernous sinus in magnetic resonance imaging]. / Diagnóstico de trombosis del seno cavernoso en imagen por resonancia magnética.

The diagnosis of the cavernous sinus thrombosis requires a careful clinical evaluation and appropriate radiological methods. In this report we describe the magnetic resonance imaging findings in a patient with the clinical diagnosis of cavernous sinus disorder and its correlation with orbital phlebography and histopathologic studies.