Signs Of Meningeal Irritation Research Articles

To Tap or Not to Tap…

A survey of the signs and symptoms of 709 children subjected to lumbar puncture on the suspicion of meningitis did not permit construction of a pattern which could identify the existence of meningitis in a suspected case. The predictive value for the symptoms of lethargy, headache, and convulsion associated with fever became meaningful only when the symptoms were associated with one or more signs of meningeal irritation.

CNS leukemia mimicking multifocal leukoencephalopathy.

With the advent of modern chemotherapy and subsequent alteration of the natural course of acute lymphocytic leukemia over the last decade, central nervous system (CNS) leukemia has emerged as a significant therapeutic problem. 1 We have recently treated a patient with acute lymphocytic leukemia who had tremor, ataxia, and transient hemiparesis without classic signs of meningeal irritation. A diagnosis of multifocal leukoencephalopathy was entertained, but lumbar puncture revealed the true nature of the disease to be leukemic involvement of the CNS. A complete response to intrathecal methotrexate was obtained. Report of a Case A 4-year-old white boy was examined, and acute lymphocytic leukemia was diagnosed in June of 1966. He had obtained his fourth complete remission on vincristine sulfate, prednisone, and daunomycin in August 1968 and was being maintained on once-monthly doses of these drugs. Two weeks prior to admission in association with an upper respiratory infection, the parents

Mollaret's Meningitis: A Case Report and Review of the Literature

Mollaret's meningitis is defined as a benign recurrent aseptic meningitis characterized by three to ten episodes of fever and signs of meningeal irritation lasting between 2 to 5 days, associated with spontaneous recovery. Mollaret in 1944 described this rare form of self limiting aseptic recurrent benign meningitis. It is an extremely rare condition. Till 2002 approximately 50 cases of recurrent HSV meningitis have been described in the United States and in Europe. Here a report of a patient with recurrent meningitis, which resembles the criteria of Mollaret's Meningitis, is presented. doi: 10.3329/taj.v17i1.3489 TAJ 2004; 17(1) : 41-46

Childhood pneumococcal meningitis: may it begin with diarrhea and proceed with cerebral infarct?

Pneumococcal meningitis does continue to be an important cause of mortality and morbidity in childhood despite widespread vaccination. It develops thorough invasion of the meninges by the agent via bloodstream. It may manifest typical signs of meningeal irritation and even the symptoms not belonging to the central nervous system, such as diarrhea. The diagnosis is made by microscopic evaluation and culture of cerebrospinal fluid (CSF) obtained by lumbar puncture. Despite the treatment, the risk of occurrence of cerebral and neurologic complications is high. A two-month old baby girl was presented to our outpatients' clinic because of fever and diarrhea; she was diagnosed with pneumococcal meningitis and developed cerebral infarct during surveillance. The reason why we presented this patient is to highlight that meningitis due to pneumococ, one of the most common causing agents in childhood meningitis, may have clinical presentations other than expected. Key words: Pneumococcal meningitis; cerebral infarct; infant. DOI: 10.3329/bjms.v10i1.7320 Bangladesh Journal of Medical Science Vol.10 No.1 Jan 2010 pp.52-56

Meningeal involvement with metastatic carcinoma of the breast treated with intrathecal methotrexate.

A patient with signs of meningeal irritation was found to have tumor cells in the cerebrospinal fluid which were metastatic from a small primary carcinoma in the left breast. Treatment with intrathecal methotrexate in dosages up to 1 mg/kg of body weight together with systemic injections of citrovorum factor was tolerated without adverse effect. Her neurologic manifestations cleared and the cerebrospinal fluid changes reverted to normal. The patient died 5 months later of advancing systemic disease with pulmonary involvement. There was no clinical recurrence of any neurologic disorder. Since the blood-brain barrier impedes the entrance of methotrexate into the central nervous system, the importance of administration by the intrathecal route with a large injection volume is emphasized.

PRELIMINARY ANTIBIOTIC THERAPY IN BACTERIAL MENINGITIS.

Bacterial meningitis is not always easy to recognize clinically. 1 Signs of meningeal irritation are often preceded by an upper respiratory infection, otitis media, or fever. Until they appear, meningitis may be unsuspected and antibiotic agents may be administered before a diagnostic lumbar puncture is performed. Exact information about such preliminary treatment is difficult to obtain. Consequently, little is known of the effects of such early therapy on the course of the disease. To evaluate the effect of preliminary antimicrobial therapy, the experience with bacterial meningitis at Wilford Hall USAF Hospital was reviewed. Inasmuch as the patients were seen at a military medical facility during the entire course of the disease, it was possible to reconstruct the early phases of the illness and to determine which patients had received antibiotic therapy before meningitis was recognized. Clinical Material Seventy patients with nontuberculous bacterial meningitis seen during the seven-year period from February

A clinical, epidemiologic and laboratory investigation of aseptic meningitis during the four-year period, 1955-1958. I. Observations concerning etiology and epidemiology.

ASEPTIC meningitis1 is a clinical syndrome encompassing a group of illnesses that includes and is clinically indistinguishable from nonparalytic poliomyelitis. The principal features are fever and signs of meningeal irritation, with cerebrospinal-fluid findings of pleocytosis, increased protein, normal sugar and absence of bacteria. Among infectious agents, viruses have been most frequently associated with this syndrome. In recent years the relation of some of the newly recognized members of the enterovirus group2 to the aseptic-meningitis syndrome has been established by isolation in tissue culture of viruses from patients with these illnesses. This group of viruses has epidemiologic and laboratory attributes closely . . .

Herpes zoster encephalitis

This report summarizes the experience with fourteen cases of herpes zoster encephalitis. The pathology is discussed on the basis of reports in the literature. It has been noted that the pathologic changes usually are in the nature of a disseminated encephalomyelitis, with lymphocytic infiltration and partial demyelination. The clinical manifestations are described. In the majority of the cases the clinical picture reflected an acute meningoencephalitic insult, with fever, change in the sensorium and signs of meningeal irritation. The clinical course was usually short, with recovery in one to three weeks. The spinal fluid was usually clear, with an increase in cells, predominantly lymphocytes. An increase in the protein content was noted in slightly more than half the cases. The sugar content was generally normal and cultures were sterile. Weak first zone colloidal gold curves were obtained in two of the cases. Electroencephaograms were obtained in three cases, in two of which the tracings were abnormal. No deaths occurred in this series during the acute phase of the disease. In a follow-up study of nine patients, six escaped without neurologic residua and three showed sequelae. In two of the latter patients abnormal electroencephalograms and abnormal colloidal gold curves were obtained early in the disease. Of special interest was the occurrence of a varicelliform eruption in four patients. The relationship between herpes zoster and varicella is discussed. Treatment was in the main symptomatic. The use of hormonal therapy merits further investigation.

Histoplasma Meningitis

Histoplasmosis tends to mimic tuberculosis in most of its manifestations; however, involvement of the central nervous system with Histoplasma capsulatum has been rarely recorded. It has been suggested that it might be more frequently found if autopsies of fatal histoplasmosis cases were done with more attention to examination of the brain. 1-2 Schulz 1 reviewed 120 autopsied cases of histoplasmosis and found Histoplasma involvement of the brain or meninges in 12 of them. Similarly, Shapiro, Lux, and Sprofkin 2 found miliary granulomas, focal destructive lesions, or leptomeningitis in 6 of 11 autopsies of patients who died of this disease. Only 5 cases of clinical meningitis ascribed to H. capsulatum have been recorded to our knowledge. Duarte, 3 in 1945, reported the case of a 23-year-old woman with headache, photophobia, nausea, and vomiting but no signs of meningeal irritation. At autopsy, the patient had a basilar meningeal exudate and lesions in

Vertebral Osteomyelitis and Urinary-Tract Infection

Osteomyelitis of the vertebral column following urinary tract infection is an uncommon clinical syndrome. To the best of our knowledge, since Carson's original report 1 in 1931, only 48 additional cases have been reported, 2-21 the majority of these cases followed urinary-tract instrumentation or other operative procedures. In approximately 25% of the cases, the infection occurred spontaneously. Following urinary-tract infection, persistent back pain, unexplained pleuritic and abdominal pain, and signs of meningeal irritation should alert the physician to the possible development of spinal osteomyelitis. The purpose of this communication is to report an additional case, again illustrating the variable clinical mainfestations of this interesting syndrome. Report of Case A 57-year-old Negro man entered Mercy Hospital for the first time on April 2, 1959, complaining of chills, fever, and back pain. The patient gave a long history of urethral stricture, and had undergone dilatation 4 days prior to admission. Twenty-four hours

Recognition and Treatment of Intracranial Manifestations of Leukemia

One of the prime objectives in the therapy of acute childhood leukemia is to maintain the patient symptom-free and capable of enjoying normal activity. The development of neurologic complications poses a serious threat to this aim. Leukemia involving the central nervous system may be manifested by symptoms and signs of meningeal irritation and increased intracranial pressure, seizures, and/or cranial nerve palsies. Not infrequently patients who have had no symptoms or signs of central nervous system involvement during life may at necropsy be found to have widespread infiltrative lesions involving the meninges and brain. Since orally administered antimetabolites apparently do not penetrate the blood-cerebrospinal fluid barrier in sufficient concentrations to prevent or control such complications, therapy in the past has included steroids and irradiation to the skull. The beneficial effects of these modes of therapy may be quite short in duration. 1 Recently, Burchenal and co-workers 2 described a dramatic beneficial

Isolation of ECHO virus type 6 during outbreak of seasonal aseptic meningitis.

• Symptoms of aseptic meningitis occurred in 17 children and in 7 young adults out of 500 inhabitants of a village in July, 1955. Seven boys were hospitalized, and all had fever, headache, signs of meningeal irritation, and gastrointestinal complaints. Pain, lethargy, mild muscular weakness, and altered reflexes were present in some cases. Improvement was rapid, and all patients were discharged well, within 3 to 10 days, with no residual findings except occasional slight muscular weaknesses and minimal hamstring spasm. Laboratory observations included detailed virus studies of the cerebrospinal fluid, blood, throat swabs, and fecal specimens. No rise of poliovirus neutralizing antibody was demonstrable in any of the patients, but in all there were rises in circulating antibody to ECHO (enteric cytopathogenic human orphan) type 6 virus. Specific antibody appeared on the fifth day of illness and was still present after seven months, when the only residual finding was absence of the abdominal reflexes in two patients. The virus was isolated, and evidence of its etiological role is given. The disease could not be distinguished clinically from preparalytic poliomyelitis when the patients were admitted to the hospital. There are indications that epidemics of this kind are not unusual or isolated occurrences.

Low cerebrospinal fluid sugar in meningeal carcinomatosis.

Case Reports1 August 1956LOW CEREBROSPINAL FLUID SUGAR IN MENINGEAL CARCINOMATOSISJ. R. D. BAYNE, M.D., P. W. DARBY, M.B., B.S.J. R. D. BAYNE, M.D.Search for more papers by this author, P. W. DARBY, M.B., B.S.Search for more papers by this authorAuthor, Article, and Disclosure Informationhttps://doi.org/10.7326/0003-4819-45-2-285 SectionsAboutPDF ToolsAdd to favoritesDownload CitationsTrack CitationsPermissions ShareFacebookTwitterLinkedInRedditEmail ExcerptThe value of the sugar content of the cerebrospinal fluid in cases of meningeal involvement by metastatic carcinoma is not widely appreciated. Metastatic involvement of the central nervous system is not uncommon, occurring in 2 to 6% of most reported series of cancer. Lesse and Netsky,1however, found central nervous system involvement in 35% of a series of cases in which the brain was examined. Many of these cases were asymptomatic, particularly where metastasis was limited to the dura, but in 10% central nervous system signs were the first to appear. Headache and signs of meningeal irritation were surprisingly uncommon;...Bibliography1. LesseNetsky SMG: Metastasis of neoplasms to the central nervous system and meninges, Arch. Neurol. and Psychiat. 72: 133, 1954. CrossrefGoogle Scholar2. GlobusMeltzer JHT: Metastatic tumors of the brain, Arch. Neurol. and Psychiat. 48: 163, 1942. CrossrefGoogle Scholar3. MerrittFremont-Smith HHF: The cerebrospinal fluid, 1937, W. B. Saunders Co., Philadelphia. Google Scholar4. DodgeSayreSvien HWGPHJ: Sugar content of the cerebrospinal fluid in diffuse neoplastic involvement of the meninges, Proc. Staff Meet., Mayo Clin. 27: 259, 1952. MedlineGoogle Scholar5. Murphy EF: Cerebrospinal fluid in carcinomatosis of the meninges, Lancet 1: 231, 1955. CrossrefGoogle Scholar This content is PDF only. To continue reading please click on the PDF icon. Author, Article, and Disclosure InformationAffiliations: *Received for publication May 6, 1955.Requests for reprints should be addressed to P. W. Darby, M.D., Central Histological Laboratory, Whittington Hospital, Archway Wing, Archway Road, London, N. 19, England. PreviousarticleNextarticle Advertisement FiguresReferencesRelatedDetails Metrics Cited byCarcinomatous Meningitis, with Special Reference to Low Chloride Concentration in the Cerebrospinal FluidRelationship between cell type, glucose concentration, and response to treatment in neoplastic effusionsOcular Signs in Diffuse Carcinomatous Meningitis* 1 August 1956Volume 45, Issue 2Page: 285-288KeywordsCarcinomatosisCentral nervous systemCerebrospinal fluidDiarrheaHeadachesMeningesMeningitisPathologistsProteinsTuberculosis ePublished: 1 December 2008 Issue Published: 1 August 1956 PDF downloadLoading ...

Encephalitis following smallpox vaccination.

VACCINATION against smallpox carries with it a known risk of postvaccination encephalitis. The rate of incidence of this complication is not constant. The numerous reports of encephalitis following smallpox vaccination show that the incidence varies not only in different localities but also in the same locality in different years. In Tyrol, for instance, a rate of 1 case of encephalitis to 641 vaccinations was reported in 1929, while an incidence ratio of 1: 4570 was observed in 1927.1In the United States, 1 case in 350 vaccinations occurred in the years 1928 to 1930, but a ratio of 1: 1000 was recorded in a large city in 1930.2 A presumptive diagnosis of postvaccination encephalitis is usually made on the basis of the onset, 7 to 14 days after vaccination, of an acute illness, with fever, headache, vomiting, change in the mental state, signs of meningeal irritation, paralyses, and

Periarteritis nodosa; report of a case of apparent recovery in a nine-year-old boy during cortisone therapy.

PERIARTERITIS nodosa has no typical course. It resembles various other diseases and is seldom proved during life. It is therefore an alternative to be considered in diagnosing many of the illnesses of childhood. 1 Analyzing 42 cases of periarteritis nodosa in children (as found in the literature) Keith and Baggenstoss 2 listed the following symptoms in order of frequency: fever, usually intermittent; leucocytosis; abdominal pains; rheumatic pains; renal disease; general weakness; convulsions; tachycardia; anemia; purpuric rash; other rashes, chiefly urticaria; hypertension; tonsillitis or sore throat; headaches; intestinal hemorrhage; peripheral gangrene; signs of meningeal irritation; palpable nodules. The small number of cases recorded (less than 500 among adults, less than 60 among children) may be attributed partly to the rarity of the disease and partly to the difficulties of recognition. Even when diagnosis is established, death usually follows. No specific therapy is known. In this disease of the

Benign Arachnoid Cysts of the Posterior Fossa

Benign, monolocular cysts of the arachnoid in the posterior fossa are apparently quite rare. Sporadic reports of isolated cases of this type of lesion have appeared in the literature frequently under titles suggesting that their origin is due to inflammation. The first clear description of such a lesion was found in a report by Craig, 2 in 193~, under the name of chronic arachnoiditis. In his Case I he described a abnormality found in the midline of the posterior fossa, overlying the cerebellum and 4th ventricle. This case, however, was presented with ~ others, all of which were discussed as individual examples of a distinct, clinical entity. In one, a multilocular cyst, with fibrous and adhesive changes, was found in the posterior fossa of a 9-year-old child, following a prolonged, severe, pulmonary infection, complicated by signs of meningeal irritation. The other patient had a noncystic, posterior fossa The absence of cyst formation in one and the multilocular nature of the cyst in the other, especially with the evidence of acute inflammation, led us to consider the latter lesions dissimilar to the subject of this report. Reference was made by Bucy 1 in 1946 to a similar lesion in which a small tuft of choroid plexus was found attached to the cyst wall. This ectopic ehoroid plexus was held to be responsible for the fluid within the cyst, which, in compressing the vermis and the 4th ventricle, produced symptoms of intracranial hypertension. A similar lesion was described in 1946 by Thompson, 7 who employed the term cystic cerebellar araehnoiditis. In spite of this nomenclature, which implies an inflammatory origin, the etiology of the lesion was at tr ibuted to t rauma sustained by the patient in a parachute jump. In 1948 Kaplan 5 briefly reviewed the reports of Craig 2 and Thompson 7 and presented ~ similar cases of his own. Much confusion exists in regard to the etiology of these lesions. In addition to the suggested role of trauma, 7 it has been implied that they are secondary to inflammation 2 and, also, tha t they are developmental anomalies. 5 Review of the literature has failed to reveal reports of similar cases other than the 5 mentioned above. The rari ty of this lesion, and the divergent opinion regarding its etiology, prompted the present report.

Traumatic Pneumocephalus

Prior to the advent of radiologic diagnosis, only one case of traumatic pneumocephalus had been reported. Extracranial pneumatocele, characterized by the dissection of air through the subaponeurotic tissues of the scalp, has long been recognized, but its intracranial counterpart, following fracture of the paranasal sinuses or mastoids, was not so accessible to the usual methods of diagnosis. Since the report of Luckett in 1913, many cases of pneumocephalus have been recorded, and major contributions such as those of Dandy and Lewis have appeared. The following case presents evidence of the immediate development of pneumocephalus following skull fracture, a somewhat unusual finding. A well developed white male was attacked by thieves as he stopped to change a tire early in the morning of April 10, 1948. He evidently was struck about the head and face by some blunt object. He was found unconscious on the street shortly after the beating and was brought immediately to Wesley Memorial Hospital. Films of the skull and facial bones taken probably four or five hours after injury were not entirely satisfactory because of the patient's disoriented condition. They revealed, however, various linear fractures in the vault, chiefly on the left, with multiple fracture lines entering the base of the skull in the region of the sphenoid yoke and the cribriform plate. Fracture of the lateral wall of the right maxillary sinus, with dense clouding of this sinus, was also observed. A large amount of air was seen within the subarachnoid space, both in the basal cisterns and surrounding the cerebral convexities. The lateral ventricles were well delineated by air (Fig. 1). Air was also present in the subdural space about the falx (Fig. 2). Physical examination on entry to the hospital showed edema and ecchymosis of the periorbital tissues. The left pupil was larger than the right, and there was no evidence of light perception by the left eye. A large hematoma was present over the left temporal bone, and there were a few small lacerations, the largest involving the left ear. Dry blood was seen in the nasal cavity, but no cerebrospinal fluid rhinorrhea or otorrhea was observed at this time. There were no cranial nerve motor changes, and generally the reflexes were normal; no signs of meningeal irritation were present. Blood pressure was 130/78. Laboratory findings were not significant. By April 11 the patient was fully conscious. He received penicillin and sulfonamides from the time of admission to April 18. Parenteral fluids were discontinued after the first two days, after which time he took nourishment by mouth. The blood pressure ranged from 120 to 140 systolic and from 68 to 90 diastolic. The temperature, which rose to 103° F. on April 12, subsided rapidly and remained under 99.4° to the time of discharge. Ophthalmologic examination on April 14 revealed complete blindness of the left eye, and it was concluded that the left optic nerve had been severed.

MODIFICATION OF MENINGEAL SIGNS BY CONCOMITANT HEMIPARESIS

SIGNS OF MENINGEAL IRRITATION SINCE Kernig's description 1 in 1907 of a localized pointing to meningeal disease, there has been a constantly increasing body of knowledge concerning such phenomena. It was evidently Kernig's early belief that the sign which he first described was a specific finding for epidemic cerebrospinal meningitis. This early belief was, of course, unfounded, and Kernig later corrected his statement, since the reaction is present in many other varieties of meningeal irritation. Many different, but related, signs of meningeal irritation have since been described, although none is of greater clinical importance than the Kernig leg sign. The purpose of this presentation is to point out the modification of the meningeal which frequently occurs when hemiparesis and meningeal irritation are present concomitantly. The recognition of this modification is of clinical importance, as will be shown. In addition, a study of the modification sheds further light

THE CLINICAL SIGNS OF MENINGEAL IRRITATION

Journal Article THE CLINICAL SIGNS OF MENINGEAL IRRITATION Get access JOHN E. A. O'CONNELL JOHN E. A. O'CONNELL Search for other works by this author on: Oxford Academic PubMed Google Scholar Brain, Volume 69, Issue 1, March 1946, Pages 9–21, https://doi.org/10.1093/brain/69.1.9 Published: 01 March 1946

Subarachnoid Injection of Thiamine in Cats; Unmasking of Brain Lesions by Induced Thiamine Deficiency

Summary1. Subarachnoid injection of thiamine causes rapid recovery of thiamine-deficient cats. Recovery is equally rapid when the vitamin is given intravenously or intramuscularly. 2. Moderate signs of meningeal irritation follow introduction of thiamine chloride into the subarachnoid space. 3. Thiamine deficiency may unmask symptoms due to an organic defect in the brain.