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PubMed2003

Cannabis use as described by people with multiple sclerosis.

BACKGROUND: Multiple sclerosis (MS) is one of the most common neurological diseases affecting young adults. The prevalence of MS in Alberta has been described as among the highest reported in the world, estimated at 217 per 100,000. Numerous anecdotal reports, and a few small empirical investigations have suggested that cannabis use may relieve the symptom experience of those with MS. The present study was undertaken to describe cannabis use by this patient group. Information on peoples' beliefs, practices and experiences related to use were investigated. METHODS: A questionnaire was mailed to a sample of 780 adults with MS in southern Alberta, Canada. RESULTS: Completed questionnaires were returned by 420/673 eligible subjects (response rate 62%). Mean sample age was 48 years and 75% were women. Respondents ranged from mildly to severely impaired. The majority of respondents (96%) was aware cannabis was potentially therapeutically useful for MS and most (72%) supported legalization for medicinal purposes. Forty-three percent had tried cannabis at some point in their lives, 16% for medicinal purposes. Symptoms reported to be ameliorated included anxiety/depression, spasticity and chronic pain. Reasons given for not trying cannabis were the fact that it is an illegal substance, concern about side effects and lack of knowledge on how to obtain it. CONCLUSIONS: Subjective improvements in symptom experience were reported by the majority of people with MS who currently use cannabis. Further evaluation of this substance is warranted.

Adult↗
PubMed2003

The role of CD1-mediated presentation of myelin lipids in experimental autoimmune encephalomyelitis and multiple sclerosis pathologenesis.

Multiple sclerosis (MS) is a chronic inflammatory disease of the central nervous system characterized by the destruction of the myelin sheath surrounding axons. On the basis of data from the animal model, experimental autoimmune encephalomyelitis (EAE) and the detection of myelin-reactive cells in MS patients, this destruction is thought to be due to an autoimmune T-cell-mediated response to myelin antigens. Until recently, the characterization of T-cell recognition of myelin antigens has necessarily focused on the response to myelin proteins. However, the discovery of CD1-mediated presentation of lipids and glycolipids to a variety of T-cell populations has greatly expanded the repertoire of antigens to which T cells can respond. Studies in the EAE model suggest a role for myelin lipids in disease pathogenesis. Recent characterization of the expression and function of CD1 and the responding T-cell populations does support a role for this pathway in the disease process. Furthermore, data suggest that it may be possible to modulate the disease course by targeting this pathway. Characterization of CD1-mediated presentation of lipids to T cells has only recently been investigated in MS, with most attention focusing on the expression of group I CD1 proteins in MS lesions. In light of data from the animal model, further characterization of the expression and function of group I and group II CD1 proteins is warranted, and could lead to the development of effective therapies to treat MS.

Animals↗
PubMed1999

CTLA-4 gene polymorphism may modulate disease in Japanese multiple sclerosis patients.

Multiple sclerosis (MS) is widely believed to have a T-cell-mediated autoimmune etiology. The CTLA-4 gene is a strong candidate for involvement in autoimmune diseases because it plays an important role in the termination of T-cell activation. To examine the genetic association of the CTLA-4 gene locus with MS, we analyzed the CTLA-4 gene exon 1 A/G polymorphism in 74 Japanese MS patients and 93 controls. We also investigated the possible interactions of the CTLA-4 gene polymorphism with clinical course and severity, with MRI findings, with another genetic marker-HLA antigens, and with oligoclonal bands (OCB) in the cerebrospinal fluid (CSF). The CTLA-4 exon 1 polymorphism was similar between MS patients and controls. Conversely, clinical disability was significantly more severe in AA homozygous patients than in the other patients, and the allele frequency and the phenotype frequency of the A allele were significantly higher in patients with severe-grade MRI findings of cerebral white matter than in patients with mild-grade MRI findings. The allele frequency and the phenotype frequency of the A allele were significantly higher in patients with OCB than in patients without. This CTLA-4 polymorphism may modulate the prognosis of patients with MS and may be relevant to generation of OCB in the CSF.

Abatacept↗
PubMed2004

Investigation of an inducible nitric oxide synthase gene (NOS2A) polymorphism in a multiple sclerosis population.

Multiple sclerosis (MS) is a chronic inflammatory disease of the central nervous system (CNS) affecting most commonly the Caucasian population. Nitric oxide (NO) is a biological signaling and effector molecule and is especially important during inflammation. Inducible nitric oxide synthase (iNOS) is one of the three enzymes responsible for generating NO. It has been reported that there is an excessive production of NO in MS concordant with an increased expression of iNOS in MS lesions. This study investigated the role of a bi-allelic tetranucleotide polymorphism located in the promoter region of the human iNOS (NOS2A) gene in MS susceptibility. A group of MS patients (n = 101) were genotyped and compared to an age- and sex-matched group of healthy controls (n = 101). The MS group was subdivided into three subtypes, namely relapsing-remitting MS (RR-MS), secondary-progressive MS (SP-MS) and primary-progressive MS (PP-MS). Results of a chi-squared analysis and a Fisher's exact test revealed that allele and genotype distributions between cases and controls were not significantly different for the total population (chi(2) = 3.4, P(genotype) = 0.15; chi(2) = 3.4, P(allele) = 0.082) and for each subtype of MS (P > 0.05). This suggests that there is no direct association of this iNOS gene variant with MS susceptibility.

Adolescent↗
PubMed2004

Investigation of a neuronal nitric oxide synthase gene (NOS1) polymorphism in a multiple sclerosis population.

Multiple Sclerosis (MS) is a chronic neurological disease characterized by demyelination associated with infiltrating white blood cells in the central nervous system (CNS). Nitric oxide synthases (NOS) are a family of enzymes that control the production of nitric oxide. It is possible that neuronal NOS could be involved in MS pathophysiology and hence the nNOS gene is a potential candidate for involvement in disease susceptibility. The aim of this study was to determine whether allelic variation at the nNOS gene locus is associated with MS in an Australian cohort. DNA samples obtained from a Caucasian Australian population affected with MS and an unaffected control population, matched for gender, age and ethnicity, were genotyped for a microsatellite polymorphism in the promoter region of the nNOS gene. Allele frequencies were compared using chi-squared based statistical analyses with significance tested by Monte Carlo simulation. Allelic analysis of MS cases and controls produced a chi-squared value of 5.63 with simulated P = 0.96 (OR(max) = 1.41, 95% CI: 0.926-2.15). Similarly, a Mann-Whitney U analysis gave a non-significant P-value of 0.377 for allele distribution. No differences in allele frequencies were observed for gender or clinical course subtype (P > 0.05). Statistical analysis indicated that there is no association of this nNOS variant and MS and hence the gene does not appear to play a genetically significant role in disease susceptibility.

Alleles↗
PubMed1998

Bcl-2 expressing T lymphocytes in multiple sclerosis lesions.

Multiple sclerosis (MS) is a chromatic inflammatory disease of the central nervous system. T lymphocytes play a major role in the pathogenesis of the disease. The exact mechanisms by which the inflammation is regulated in MS have not yet been defined. Studies in animal models of MS suggest that apoptosis of T cells is the main factor terminating inflammation. The process of apoptosis itself is regulated by a range of pro- and anti-apoptotic proteins. The bcl-2 gene family is an important member of these proteins. The present study investigated the expression of the anti-apoptotic protein bcl-2 in 11 chronic MS cases including five relapsing-remitting and six chronic progressive MS patients. A total of 35 lesions containing all stages of demyelinating activity were studied. The number of CD 3-positive T cells and the absolute and relative numbers of T cells expressing bcl-2 were determined by double immunocytochemistry. Bcl-2 is expressed by T lymphocytes in MS plaques. Patients with chronic progressive MS have a higher proportion of bcl-2 expressing T cells than patients with relapsing remitting disease. Highest numbers of bcl-2-positive T lymphocytes were found in remyelinating and demyelinated lesions, whereas active demyelinating lesions revealed lower numbers. These data indicate that cell-death-related proteins such as the anti-apoptotic protein bcl-2 are expressed in MS lesions and that they might have important effects on the regulation of elimination or persistence of inflammatory cells in the central nervous system.

Adult↗
PubMed2004

Expression of major histocompatibility complex class I molecules on the different cell types in multiple sclerosis lesions.

Multiple sclerosis is considered to be an immune-mediated disease of the central nervous system, characterized by chronic inflammation, primary demyelination and axonal damage. The mechanisms of demyelination and axonal injury are heterogeneous and complex. One possible mechanism is direct damage of oligodendrocytes and neurons by Class I MHC restricted cytotoxic T-cells. In this study we analyzed the expression of functional MHC class I molecule complex, consisting of alpha-chain and beta2-microglobulin, in a large sample of human autopsy material, containing 10 cases of acute MS, 10 cases of chronic active MS, 10 cases of chronic inactive MS and 21 controls. To examine the expression of MHC class I and II molecules on the different cell-types in brain, we used quantitative immunohistochemical techniques, double staining and confocal laser microscopy scans on paraffin embedded sections. We found constitutive expression of MHC class I molecule on microglia and endothelial cells. A hierarchical up-regulation of MHC class I was present on astrocytes, oligodendrocytes, neurons and axons, depending upon the severity of the disease and the activity of the lesions. MHC class II molecules were expressed on microglia and macrophages, but not on astrocytes. These data indicate that in MS lesions all cells of the central nervous system are potential targets for Class I MHC restricted cytotoxic T-cells.

Adult↗
PubMed2005

Connexin43, the major gap junction protein of astrocytes, is down-regulated in inflamed white matter in an animal model of multiple sclerosis.

Both multiple sclerosis (MS) and experimental autoimmune encephalomyelitis (EAE), its animal model, involve inflammatory attack on central nervous system (CNS) white matter, leading to demyelination and axonal damage. Changes in astrocytic morphology and function are also prominent features of MS and EAE. Resting astrocytes form a network that is interconnected through gap junctions, composed mainly of connexin43 (Cx43) protein. Although astrocytic gap junctional connectivity is known to be altered in many CNS pathologies, little is known about Cx43 expression in inflammatory demyelinating disease. Therefore, we evaluated the expression of Cx43 in spinal cords of EAE mice compared with healthy controls. Lumbar ventral white matter areas were heavily infiltrated with CD11beta-immunoreactive monocytes, and within these infiltrated regions loss of Cx43 immunoreactivity was evident. These regions also showed axonal dystrophy, demonstrated by the abnormally dephosphorylated heavy-chain neurofilament proteins. Astrocytes in these Cx43-depleted lesions were strongly glial fibrillary acidic protein reactive. Significant loss (38%) of Cx43 protein in EAE mouse at the lumbar portion of spinal cords was confirmed by Western blot analysis. Decreased Cx43 transcript level was also observed on cDNA microarray analysis. In addition to changes in Cx43 expression, numerous other genes were altered, including those encoding adhesion and extracellular matrix proteins. Our data support the notion that, in addition to damage of myelinating glia, altered astrocyte connectivity is a prominent feature of inflammatory demyelination.

Animals↗
PubMed1999

Bcl-2-expressing oligodendrocytes in multiple sclerosis lesions.

Multiple sclerosis (MS) is a chronic inflammatory disease of the central nervous system leading to selective destruction of myelin sheaths and/or oligodendrocytes. The immunological mechanisms responsible for myelin destruction and the primary target of the immune response have not yet been identified. Prior studies have reported a variable degree of oligodendrocyte preservation in actively demyelinating lesions. We have previously demonstrated that oligodendrocyte survival is heterogenous and varies between individual MS patients. Bcl-2 belongs to the group of apoptosis-associated proteins that protects cells from cell death. The purpose of the present study was to determine whether bcl-2 expression is associated with oligodendrocyte preservation observed in some early MS lesions. Double immunocytochemistry was performed with antibodies against bcl-2 and myelin oligodendrocyte glycoprotein (MOG) to identify bcl-2-expressing oligodendrocytes within MS lesions from 43 patients. The number of bcl-2-positive oligodendrocytes was determined depending on the lesion demyelinating activity and the disease course of the patients. The number of bcl-2-expressing oligodendrocytes increased within demyelinating lesions compared to the periplaque white matter, with highest numbers in remyelinating lesions. There was a significant association between the presence of bcl-2-positive oligodendrocytes and the presence of remyelination. The highest proportion of bcl-2-positive oligodendrocytes was observed in a subgroup of patients with relapsing-remitting disease course. The expression of apoptosis-associated proteins may contribute to oligodendrocyte preservation or loss in MS lesions.

Adolescent↗
PubMed2006

Unusual ocular motor findings in multiple sclerosis.

In multiple sclerosis (MS), nystagmus or internuclear ophthalmoplegia (INO) are the usual ocular motor dysfunctions. However, in patients with focal brainstem lesions, other rare manifestations may be observed, such as an isolated ocular motor nerve palsy or complex ocular motor disturbances. We report five MS patients with unusual ocular motor disturbances (bilateral third nerve palsy [n = 2], opsoclonus, Horner's syndrome and one-and-a-half syndrome). We discuss possible correlations between clinical disturbances and MRI abnormalities. Patients were seen in two MS centres. They had a confirmed diagnosis of MS and underwent a brain MRI and a complete neuro-ophthalmological work-up. In one case (opsoclonus), ocular motor manifestations were the first manifestation of MS. In the other four cases they occurred 3 months (Horner syndrome), 6 years and 12 years (bilateral third nerve palsy) and 2 years (one-and-a-half syndrome) after the disease onset, respectively. Four out of five patients were still in a relapsing-remitting form of MS. In the opsoclonus case, there was no evidence of a brainstem lesion. A gadolinium-enhanced lesion (2 cases) or a new T2-weighted lesion located in the brainstem correlated with the clinical presentation. All patients completely or partially recovered after corticosteroid infusions. Our study shows some rare or previously undescribed complex ocular motor symptoms in MS.

Adjuvants, Immunologic↗
PubMed2004

Cytokine-induced enhancement of autoimmune inflammation in the brain and spinal cord: implications for multiple sclerosis.

UNLABELLED: Multiple sclerosis and experimental autoimmune encephalomyelitis (EAE) are autoimmune inflammatory diseases in which cytokines are intimately involved. Here we test the hypothesis that injection of pro-inflammatory cytokines, tumour necrosis factor-alpha (TNFalpha) and interferon gamma (IFNgamma) into the brain of animals in the prodromal phase of EAE significantly enhances inflammation in the central nervous system (CNS). We were particularly interested to learn whether a local increase in cytokines influenced the pathology locally, or more extensively, within the CNS. EAE was induced in female adult Lewis rats. Eight days post-inoculation, TNFalpha or INFgamma was injected into one cerebral hemisphere. Days 11 and 13 post-inoculation (3 and 5 days after the injection of cytokine) inflammation was quantified by the number of perivascular cuffs and the degree of major histocompatibility complex (MHC) class II expression by microglia. Normal animals injected with cytokines, and EAE animals with saline injection served as controls. RESULTS: microglial activation was increased three- to fourfold in the brain and eightfold in the spinal cord (P </= 0.05); lymphocyte invasion was increased sixfold in the brain and three- to fourfold in the spinal cord (P </= 0.01) following injections of TNFalpha or INFgamma in EAE animals compared with controls. Significant axonal damage was observed in white matter associated with the perivascular cuffs. CONCLUSION: local changes in the release of pro-inflammatory cytokines within the brain in EAE results in the widespread enhancement of autoimmune inflammation within the brain and cord, and exacerbation of clinical symptoms.

Animals↗
PubMed1998

Golli-MBP gene in multiple sclerosis susceptibility.

Multiple sclerosis (MS) is an oligo- or polygenic disease but no specific susceptibility genes have been identified so far. In the Finnish population we have previously found evidence for linkage between MS and the myelin basic protein gene (here called Golli-MBP gene) suggesting that either Golli-MBP or another gene in its vicinity contributes to MS suceptibility. Here we have screened the Golli-MBP gene for nucleotide variations and carried out multipoint association analyses in a Finnish case-control data-set as well as in an independent data-set composed of 151 MS families from Finland and Sweden. In both data-sets we found association between MS and alleles in the 1.27 kilobase (kb) range at a tetranucleotide repeat element (TGGA)n which is located 1 kb upstream of the MBP exon 1. Haplotype analyses suggested that the MS-associated 1.27 kb alleles can be split into predisposing and non-predisposing variants and provided evidence that the candidate DNA region contributing to MS susceptibility should be located at the Golli-MBP gene within a 20-25 kb segment that was conserved in the predisposing haplotypes. These findings suggest a role for the Golli-MBP locus in MS susceptibility, at least in a subset of patients, and serve as a basis for highly focused attempts to identify predisposing mutation(s).

Adult↗
PubMed1995

Alterations in peripheral blood mononuclear cell cytokine production in response to phytohemagglutinin in multiple sclerosis patients.

Multiple sclerosis (MS) is an autoimmune demyelinating disorder of the central nervous system (CNS). The disease is characterized by inflammatory lesions in the white matter of the CNS, consisting of a specific immune response to the myelin sheath. We investigated peripheral blood mononuclear cell (PBMC) cytokine production by enzyme-linked immunosorbent assays of 21 MS patients and 19 age-matched normal controls in response to the T-cell mitogen phytohemagglutinin (PHA). Peripheral blood mononuclear cells were cultured in medium alone or in medium with 5 micrograms of PHA per ml for 48 h, and culture supernatants were collected for analysis. Cytokines selected for study were interleukin-10 (IL-10), gamma interferon (IFN-gamma), IL-2, and IL-4. All cytokine activities described were expressed as concentrations per 500,000 cells. We found that 48% (10 of 21) of the MS patients produced small but detectable levels of IL-10 in medium alone, compared with 26% (5 of 18) of the controls. We found that the MS patients produced significantly higher quantities of IL-10 protein than the controls in response to PHA (mean supernatant concentrations of IL-10 for patients and controls, 421 and 204 pg/ml, respectively [P < 0.05]). No significant differences were detected in the production of IL-2, IFN-gamma, and IL-4 between patients and controls in response to PHA, although patients appeared to display a trend toward decreased production of IFN-gamma.

Adult↗
PubMed1985

Responses to paired onset stimuli: implications for the delayed evoked potentials in multiple sclerosis.

In multiple sclerosis (MS), demyelination is reported to be patchy and randomly distributed across the optic nerve, and a double peaked or broadened shape of the peaks of the pattern evoked potential would be expected. We tested quantitatively this hypothesis for our routinely recorded responses of MS patients. There was no significant broadening of the peak shape in the 75 prolonged latency responses. In order to simulate the patchy character of the affection of the optic nerve in MS, we tested 2 healthy subjects with a stimulus consisting of 2 presentations of a checkerboard pattern to different parts of the visual field, but with an adjustable onset asynchrony. It was found that, when the asynchrony was small (less than 40 msec) the second of the two stimuli did not contribute to the response. This suppression of the second response could be observed even when the second stimulus, by increasing its contrast, was made to evoke a much larger response than the first stimulus, when presented separately. Inhibition of the second response seems to explain the lack of wave shape alteration in the responses of MS patients, which would be expected on the basis of the patchy character of the demyelination. The responses from the fastest conducting fibres seem to determine the response, and inhibit the responses of the demyelinated fibres. From this, it can be concluded that a delayed response would be expected only in patients in whom a considerable number of the fibres of the optic nerve is affected by the demyelination. This seriously limits the sensitivity of the method for early diagnosis.

Adult↗
PubMed2005

Oral health status and temporomandibular disorders in multiple sclerosis patients.

Multiple sclerosis (MS) is an inflammatory disease of unknown etiology involving the central nervous system. Certain clinical manifestations affect the oro-facial region. Three in particular should be of interest to the dentist: trigeminal neuralgia, sensory neuropathy of the trigeminal nerve and facial palsy. The aim of this study was to determine the oral health status, the frequency of subjective symptoms and temporomandibular disorders (TMD) subtype according to Research diagnostic criteria for temporomandibular disorders (RDC/TMD) among MS patients. Examinees in this study were 50 patients suffering from MS, who were at least once treated during their disease in the Clinic Hospital Center, Rijeka, Clinic for Neurology. All examinees had to meet the diagnostic criteria for clinically and laboratory confirmed MS, according to Poser. The results show the difference in mean DMFT (decayed, missing, filled teeth) between MS and the control group. The number of decayed and missing teeth was higher, but the number of filled teeth was significantly lower in MS group. Eighty-two per cent of the subjects with MS had a least one symptom of dysfunction compared with 24% of the subjects in the healthy control group. In the present study, pain, the pain during mouth opening, the difficulty with mouth opening and temporomandibular joint (TMJ) sounds were more commonly reported in the MS group than in the control group. This study shows a statistically significant excess of dental caries and temporomandibular disorders among MS patients compared with the control group. These results suggest that MS is a possible etiological factor in temporomandibular disorders.

Adult↗
PubMed2005

A primary care-based needs assessment of people with multiple sclerosis.

BACKGROUND: Multiple sclerosis (MS) is a common cause of chronic progressive neurological disability where reduction in quality of life is an important feature. Many GPs have MS patients with a range of disabilities. Little is known about the supply of medical and community services and how this compares with demand. AIM: We aim to describe a community based sample of MS patients and investigate how disease characteristics, benefits, services accessed and perceived needs relate to sense of wellbeing. DESIGN: Cross-sectional survey. SETTING: Participants were recruited from a representative network of 30 GP practices across Northern Ireland. METHOD: MS patients answered a professionally administered questionnaire and agreed to their medical records being examined. Information was collected about their medical condition, sociodemographic characteristics, receipt of benefits and services, perceived needs and sense of wellbeing. RESULTS: Of the 149 participants, 23% were mildly affected (Kurtzke's Expanded Disability Status Scale [EDSS] 0-4.5), 41% were moderately disabled (EDSS 5.0-6.5) and 36% were severely disabled (EDSS 7.0-9.5). Disability was related to employment, receipt of benefits and services. Physiotherapy was a commonly perceived need. Other perceived needs differed between the moderately and severely disabled groups. Scores relating to wellbeing were related to disability and perceived needs. CONCLUSIONS: The relationship between use of medical and community services and disability is important for planning service provision. We have shown that perceived needs are related to wellbeing. In a progressive illness these developing needs could be anticipated.

Adult↗
PubMed2001

Transected neurites, apoptotic neurons, and reduced inflammation in cortical multiple sclerosis lesions.

Multiple Sclerosis (MS) is an inflammatory demyelinating disease of the central nervous system that causes motor, sensory, and cognitive deficits. The present study characterized demyelinated lesions in the cerebral cortex of MS patients. One hundred twelve cortical lesions were identified in 110 tissue blocks from 50 MS patients. Three patterns of cortical demyelination were identified: Type I lesions were contiguous with subcortical white matter lesions; Type II lesions were small, confined to the cortex, and often perivascular; Type III lesions extended from the pial surface to cortical layer 3 or 4. Inflammation and neuronal pathology were studied in tissue from 8 and 7 patients, respectively. Compared to white matter lesions, cortical lesions contained 13 times fewer CD3-positive lymphocytes (195 vs 2,596/mm3 of tissue) and 6 times fewer CD68-positive microglia/macrophages (11,948 vs 67,956/mm3 of tissue). Transected neurites (both axons and dendrites) occurred at a density of 4,119/mm3 in active cortical lesions, 1,107/mm3 in chronic active cortical lesions, 25/mm3 in chronic inactive cortical lesions, 8/mm3 in myelinated MS cortex, and 1/mm3 in control cortex. In active and chronic active cortical lesions, activated microglia closely apposed and ensheathed apical dendrites, neurites, and neuronal perikarya. In addition, apoptotic neurons were increased significantly in demyelinated cortex compared to myelinated cortex. These data support the hypothesis that demyelination, axonal transection, dendritic transection, and apoptotic loss of neurons in the cerebral cortex contribute to neurological dysfunction in MS patients.

Adolescent↗
PubMedDate not supplied

[Historical aspects of multiple sclerosis].

INTRODUCTION: Multiple sclerosis (MS) is one of the most common diseases of the central nervous system (CNS) in young adults. MS is the most common disorder of the central nervous system in young people living in temperate climate regions. Although a few references to possible cases of the disease come from the xiii century, its scientific observation and systematic study only started in the late xix century. DEVELOPMENT: Robert Carswell e Jean Cruveilhier were the first investigators to document the pathological lesions while the clinical picture was first studied by Charcot. In spite of a huge number of infectious agents has been proposed for the etiology of MS and a genetic susceptibility trait recently defined, the ultimate cause of the disease remains to be determined. The development of diagnostic criteria sets, clinical disability scales and image methods in the latter half of the last century has provided investigators with useful research tools allowing unprecedented advances. In the last 30 years ACTH and corticosteroids have been employed as treatment for MS relapses. Starting in 1993 a new class of drugs called disease modifying agents, such as interferon beta and more recently glatiramer acetate, was introduced with encouraging results. CONCLUSIONS: MS is postulated to be a cell mediated autoimmune disease directed against CNS myelin components and characterized by inflammation and chronic demyelination. This paper is a review of the principal most significant events in the search for knowledge of the disease in the world.

Diagnosis, Differential↗