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PubMedDate not supplied

Clinical manifestations and treatment outcome of optic neuropathy in thyroid-related orbitopathy.

BACKGROUND AND OBJECTIVE: To investigate the incidence and outcome of optic neuropathy associated with thyroid-related orbitopathy. PATIENTS AND METHODS: All patients diagnosed as having optic neuropathy associated with thyroid-related orbitopathy who underwent treatment for optic neuropathy between January 1, 1999, and March 1, 2003, were reviewed. Demographic and clinical data were extracted from the oculoplastic registry (electronic medical record). RESULTS: Optic neuropathy occurred in 20 of 595 patients with thyroid-related orbitopathy (3.4%). All patients received systemic steroids, 7 patients received orbital steroid injections, and 2 patients were treated with orbital radiotherapy. Orbital decompression was performed in all 26 orbits. Visual acuity improved from a mean of 20/150 to 20/30 (P < .001). Color vision improved from a mean of 5.2/14 to 11/14 (P = .001). The afferent pupillary defect disappeared shortly after treatment for all but 1 case, and improved in all cases. Exophthalmos decreased from 26.4 +/- 2.5 to 21.5 +/- 2.1 mm (P< .001; 95% confidence interval, 3.8 to 5.7). CONCLUSIONS: Optic neuropathy manifests rarely in patients with thyroid-related orbitopathy. Monitoring visual acuity or afferent pupillary response may be a reliable way of assessing and monitoring optic neuropathy. In this study, patients had improved visual acuity and optic nerve function after a combination of medical and surgical treatment.

Adult↗
PubMed2002

Utility of subcutaneous fat aspiration for diagnosing amyloidosis in patients with isolated peripheral neuropathy.

OBJECTIVE: To determine the value of subcutaneous fat aspiration in patients with sensorimotor peripheral neuropathy. PATIENTS AND METHODS: We retrospectively reviewed the medical records of all patients undergoing subcutaneous fat aspiration for suspected amyloidosis from January 1, 1994, through December 31,1999. We classified patients undergoing subcutaneous fat aspiration due to peripheral neuropathy into 2 groups: (A) those with isolated peripheral neuropathy and (B) those with any family history and laboratory or clinical findings typically associated with systemic amyloidosis. RESULTS: The study population consisted of 450 patients with peripheral neuropathy in whom fat aspiration was performed for suspected amyloidosis. This constituted 56% of all fat aspirations performed during the study period. Group A had 143 patients, and group B had 307 patients. None of the patients in group A had a positive subcutaneous fat aspirate, whereas 17 patients (6%) in group B had a positive subcutaneous fat aspirate (P=.002, Fisher exact test). The subcutaneous fat aspirate was most commonly positive in patients with a monoclonal protein or other clinical findings associated with amyloidosis. CONCLUSIONS: The yield of a subcutaneous fat aspirate in patients with isolated peripheral neuropathy and no other associated family history, signs, or symptoms of amyloidosis is low. Subcutaneous fat aspiration should be reserved for evaluating patients with peripheral neuropathy who also have findings associated with systemic amyloidosis.

Adipose Tissue↗
PubMed2001

Cranial and peripheral neuropathies.

An acute polyneuropathy developing over days to several weeks is most likely to be Guillain-Barré syndrome or a toxic neuropathy, although vasculitis can also present acutely. This presentation should be referred immediately for further investigation. A subacute to chronic (ie, developing over months) neuropathy with significant proximal weakness and prominent loss of reflexes is highly suggestive of chronic inflammatory demyelinating polyradiculoneuropathy. If there is a clear stepwise onset of symptoms, suggestive of multiple mononeuropathies, or significant asymmetry, vasculitic neuropathy should be considered, even in the absence of systemic vasculitis. Idiopathic chronic axonal neuropathy is an indolent, predominantly sensory neuropathy that typically occurs in older patients. Neuropathies occurring in young or middle age or with more subacute onset always warrant further investigation.

Algorithms↗
PubMed1999

Patient guide to peripheral neuropathy.

PURPOSE/OBJECTIVES: To describe a booklet used to educate patients who experience peripheral neuropathy secondary to neurotoxic chemotherapy treatment. DATA SOURCES: Journal articles, neurologic physical assessment, symptom management books. DATA SYNTHESIS: The booklet defines peripheral neuropathy, the types of nerves most often affected, common causes and symptoms, and management strategies with an emphasis on safety issues. It contains a list of referral sources for additional management information and a glossary of terms related to peripheral neuropathy. CONCLUSIONS: The booklet is useful for patients in their daily management of peripheral neuropathy that has occurred as a side effect of neurotoxic chemotherapy treatment. IMPLICATIONS FOR NURSING PRACTICE: Nurses can use this information to educate patients and their caregivers about peripheral neuropathy. The booklet offers strategies to manage this side effect and maintain a safe home environment and workplace. It also offers sources of information and referrals that may benefit patients with peripheral neuropathy.

Antineoplastic Agents↗
PubMedDate not supplied

[Measurement of antiganglioside autoantibodies by immunodot-blot assay: clinical importance in peripheral neuropathies].

We retrospectively evaluated measurement data and clinical relevance of autoantibodies to gangliosides in peripheral neuropathies (PN). The IgG and IgM antiganglioside autoantibodies were determined by our own immunodot-blot assay on membrane and by enzyme-linked immunosorbent assay (Elisa) in sera of 1,342 patients with peripheral neuropathies. Anti-GM1 and anti-GD1b autoantibodies formed a part of the normal autoantibody repertoire and were common place in 12% of normal subjects and in 14% of disease control groups. Polyclonal IgM antiganglioside autoantibodies were detected in chronic PN, polyclonal IgG antiganglioside autoantibodies were detected in acute PN. Polyclonal IgM anti-GM1 and anti-GD1b autoantibodies were detected in 35 patients out of 48 with treatable multifocal motor neuropathy with persistent conduction blocks. These autoantibodies well discriminated between suspected motor peripheral neuropathies and motor neuron diseases (sensitivity 73%, specificity 83%, positive predictive value 60%, negative predictive value 91%). Monoclonal IgM autoantibodies reacted strongly with gangliosides in 15 patients out of 77 with M-IgM neuropathy (19%). M-IgM autoantibodies differed in their fine specificities with different principal target antigens as demonstrated with cross-reactivity. Such findings provide further evidence for a relationship between neurological syndromes and antiganglioside antibody profiles and also suggest that different gangliosides could be principal target antigens such as GM1, GD1b, GT1b, GD1a or GM2. Polyclonal IgG anti-GM1 and anti-GD1b autoantibodies were detected in 21 patients out of 22 with acute motor axonal Guillain-Barré syndrome with antecedent of infection by Campylobacter jejuni, polyclonal IgG anti-GQ1b autoantibodies in 9 patients out of 10 with Miller-Fisher syndrome. Detection of antiganglioside autoantibodies by immunodot-blot assay which is simple and quick in testing a large panel of gangliosides has become very important in the diagnosis and in the choose of expensive therapeutic strategies in chronic or acute autoimmune neuropathies.

Acute Disease↗
PubMed1999

Overview of hereditary neuropathy with liability to pressure palsies.

Hereditary neuropathy with liability to recurrent pressure-sensitive palsies (HNPP; also called tomaculous neuropathy) is an autosomal dominant disorder that produces an episodic, recurrent demyelinating neuropathy. HNPP generally develops during adolescence, and may cause attacks of numbness, muscular weakness, and atrophy. Peroneal palsies, carpal-tunnel syndrome, and other entrapment neuropathies are frequent manifestations of this disorder. Motor and sensory nerve conduction velocities may be reduced in clinically affected patients, as well as in asymptomatic gene carriers. Pathological changes observed in peripheral nerves of HNPP patients include segmental demyelination and tomaculous or "sausage-like" formations. Because of mild overlap of clinical features with CMT1, HNPP patients may be misdiagnosed as having CMT1. HNPP and CMT1 are both demyelinating neuropathies; however, their clinical, pathological, and electrophysiological features are quite distinct. The HNPP locus maps to chromosome 17p11.2-12 and is associated with a 1.5-Mb deletion. DNA markers known to map to the region in 17p11.2-12 associated with the CMT1A duplication, including the PMP22 gene, are deleted in HNPP. The deletion breakpoints in HNPP map to the same intervals in which the CMT1A duplication breakpoints map. In one pedigree, de novo deletion of paternal origin was detected as a basis for sporadic HNPP. HNPP results from deletion of the PMP22 gene and underexpression of this locus, which is reflected in reduced mRNA and protein levels in sural nerve biopsy samples from HNPP patients. Further support for this hypothesis was provided by the identification of a nondeleted HNPP kindred in which a two base pair deletion and early termination codon within exon 1 of PMP22 was present. The possibility of genetic heterogeneity in HNPP was raised by the identification of an HNPP pedigree that did not demonstrate linkage to the region of 17p11.2-12. Hereditary neuralgic amyotrophy (familial brachial plexus neuropathy) is an autosomal dominant disorder causing painful, recurrent brachial plexopathies and maps to chromosome 17q25.

Animals↗
PubMedDate not supplied

In vivo effect of lipoic acid on lipid peroxidation in patients with diabetic neuropathy.

BACKGROUND: The diabetic state, in both humans and experimental animals, is associated with oxidative stress. Lipid peroxidation of nerve membranes has been suggested as a mechanism by which peripheral nerve ischemia and hypoxia could cause neuropathy. Lipoic acid (LA) is a powerful inhibitor of iron-dependent lipid peroxidation and reactive oxygen species. The treatment of diabetic peripheral and cardiac autonomic neuropathy with LA is based on good clinical and experimental evidence. MATERIALS AND METHODS: To investigate the magnitude of the oxidative stress, serum ceruloplasmin (Cp) and lipid peroxide (Lp) levels were measured in 10 patients with diabetic neuropathy, before and 70 days after treatment with single dose of 600 mg LA/day. For other 12 healthy age- and sex-matched control subjects the serum Cp and Lp levels were evaluated. RESULTS: Our results show that hyperglycemia is a factor for an increase in serum ceruloplasmin in patients with diabetic neuropathy compared to healthy subjects (p < 0.0001). High serum ceruloplasmin (Cp) level in patients with diabetes may be related to antioxidant defense. The treatment of diabetic neuropathy with LA does not affect significantly the serum Cp activity. The serum Lp levels after LA administration were significantly lower (p < 0.005) than those before treatment. CONCLUSIONS: The antioxidant therapy with LA improves and may prevent diabetic neuropathy. This improvement is associated with a reduction in the indexes of lipid peroxidation. Oxidative stress appears to be primarily due to the processes of nerve ischemia and hyperglycemia autooxidation.

Aged↗
PubMed2000

Electrodiagnosis of demyelinating neuropathies.

The inflammatory demyelinating neuropathies constitute a significant proportion of the acquired polyneuropathies. Major progress in finding the causes and in the treatment of these neuropathies has been made over the last decade. Early recognition is of paramount importance, because timely and appropriate treatment can largely reduce morbidity and disability. Electrodiagnosis plays a key role in the detection and characterization of the inflammatory demyelinating neuropathies. Electrodiagnostic criteria for primary demyelination have therefore been developed. They are empirically based on changes of nerve conduction parameters in populations of patients with a confirmed clinical and laboratory diagnosis of inflammatory demyelinating neuropathy. The challenge consists of defining criteria sets that are highly specific but also as sensitive as possible. Most of the hereditary demyelinating neuropathies are part of Charcot-Marie-Tooth disease type 1. The pattern of nerve conduction abnormalities usually provides valuable clues for the distinction from chronic inflammatory demyelinating neuropathies.

Action Potentials↗
PubMed2001

SITA standard in optic neuropathies and hemianopias: a comparison with full threshold testing.

PURPOSE: To compare visual sensitivity, fatigue effect, and probability plot data between Full Threshold (FT) Humphrey automated perimetry and Swedish Interactive Threshold Algorithm (SITA) standard strategies in patients with optic neuropathies and hemianopias. METHODS: Twenty-four patients with nonglaucomatous optic neuropathies and 18 patients with a relative homonymous or bitemporal hemianopia were tested with both conventional perimetry (Humphrey 24-2 program) and "back to back" SITA standard tests (SITA 1, SITA 2) to approximate the test time of the FT test conditions. Also, 28 normal subjects between the ages of 20 and 80 were tested with this protocol. The visual field quadrants with the most damage were used to evaluate any fatigue effect (i.e., possible lack of fatigue effect with SITA standard due to the shorter test time) and to compare probability plot data between FT, SITA 1, and SITA 2. Pointwise total and pattern deviation probability plot defects were weighted by degree of significance and summed. RESULTS: Test times for normal subjects were 45 seconds longer for FT than for the combined test time of SITA 1 + SITA 2. Patients' test times were 40 seconds longer for hemianopias and 90 seconds longer for optic neuropathies with FT than the combined times for two SITA tests. There were higher sensitivities found with SITA 1 compared with Full Threshold (1.06 dB, P< 0.001) and SITA 2 with Full Threshold (0.73 dB, P< 0.001) in the most damaged quadrant for the optic neuropathy patients; for the hemianopia patients the difference in values were between SITA 1 and Full Threshold (0.96 dB, P = 0.07) and between SITA 2 and Full Threshold (0.11 dB, P = 0.87). The second SITA standard test had lower sensitivity than the first SITA standard test by 0.82 dB in hemianopias and by 0.71 dB in optic neuropathy patients. Analysis of the total and pattern deviation probability plot data showed slightly more defects (number and magnitude) with SITA 1 compared to FT for both groups, but the differences were not statistically significant. CONCLUSIONS: Sensitivities were higher in patients with hemianopias or optic neuropathies using SITA standard compared with FT by approximately 1 dB. The probability plot comparison suggests SITA standard is at least as good as FT for detection of visual loss in individual examinations. However, efficacy of SITA standard for serial examinations has not yet been evaluated.

Adult↗
PubMed1998

Nonsystemic vasculitic neuropathy.

The clinical, electrophysiological and pathological features and prognosis of 9 patients with nonsystemic vasculitic neuropathy are described. Nonsystemic vasculitic neuropathy accounted for 3% of cases of biopsy proven cases of various neuropathies and formed 56% of vasculitic neuropathy. Both clinically and on electrophysiological testing, mononeuritis multiplex was the form of neuropathy in 5 patients and 3 had sensory neuropathy. All the patients had a necrotizing vasculitis on nerve biopsy. Axonal degeneration was seen in teased fibers in all the patients. Eight patients showed good functional recovery one was left with mild bilateral claw hands.

Adolescent↗
PubMed2001

[Peripheral neuropathy in cancer].

Neuropathy is a quite common finding in cancer patients. If the cancer is known, the main clinical problem is often whether the symptoms and signs are caused by metastasis or recurrence, or if the neuropathy can be related to effects of the oncological treatment. In addition to the clinical findings, radiological and neurophysiological examination can often be of considerable diagnostic help. Peripheral neuropathy may also be the first manifestation of the cancer, as in paraneoplastic neuropathies. Detecting the tumor in these cases may improve the oncological prognosis, as the neuropathy often precedes tumor symptoms by several years. A determined approach in searching for an occult cancer is necessary. The neuropathic symptoms are seldom life-threatening. However, the neuropathy may cause distressing symptoms, and symptomatic treatment and rehabilitation is often required.

Antineoplastic Agents↗
PubMed2002

Altered levels of soluble adhesion molecules in patients with rheumatoid arthritis complicated by peripheral neuropathy.

OBJECTIVE: To assess levels of 2 circulating soluble adhesion molecules, vascular cellular adhesion molecule (sVCAM) and E-selectin, in patients with rheumatoid arthritis (RA) complicated by peripheral neuropathy compared to RA patients with no neurological complications and healthy controls. METHODS: In total, 25 RA patients with peripheral neuropathy (detected by clinical examination and confirmed by electromyography and nerve conduction studies), 40 RA patients without peripheral neuropathy, and 25 controls were studied. Clinical and laboratory assessments of disease activity were carried out and levels of sVCAM-1 and E-selectin were measured by ELISA in each of the 3 groups. RESULTS: Levels of sVCAM-1 and sE-selectin were higher (p < 0.001) in RA patients with peripheral neuropathy than in patients without neuropathy and controls. Levels of sE-selectin and sVCAM-1 correlated positively with disease activity variables. Correlation was independent of age and sex. CONCLUSION: Peripheral neuropathy in patients with RA is associated with increased endothelial cell activation evidenced by elevated serum levels of sVCAM-1 and sE-selectin in this group of patients.

Arthritis, Rheumatoid↗
PubMed2002

[Anti-glycolipid antibodies in the diagnosis of autoimmune neuropathies]

Recent years have seen major progress in our understanding of the clinical pathophysiology of autoimmune neuropathies particularly with the identification and analysis of antibodies to gangliosides and related glycolipids in the serum of patients. Anti-glycolipid antibodies react with epitopes on the carbohydrate region of glycolipid molecules and can be routinely measured by standard immunoassays. In multifocal motor neuropathy, IgM anti-GM1 antibodies that cross react with GD1b and asialo-GM1 are detectable in around 50p. 100 of cases. This condition may clinically resemble certain forms of lower motor neurone disease. IgM anti-GD1b antibodies are found in IgM paraproteinaemic neuropathy characterised by profound sensory ataxia. In the anti-myelin associated glycoprotein (anti-MAG) IgM paraproteinaemic neuropathy, antibodies also react with the acidic glycolipids, sulphated glucuronyl paragloboside and its higher lactosaminyl homologue (SGPG and SGPLG). Thus a variety of chronic syndromes can be defined by their anti-glycolipid antibody profile. In Guillain-Barré syndrome, anti-GM1, GM1b, GD1a and GalNAc-GD1a antibodies are found in patients with acute motor axonal neuropathy (AMAN) and anti-GQ1b IgG antibodies are a very sensitive and specific marker for the Miller Fisher syndrome. Many other anti-glycolipid antibodies are being increasingly identified in other neuropathy subtypes. The article will summarise existing clinical and serological information in this field.

Journal Article↗
PubMed2002

[Chronic inflammatory demyelinating neuropathies and their variants]

The Chronic Inflammatory Demyelinating Polyradiculoneuropathies (CIDP) constitute a syndrome whose incidence is difficult to evaluate, and is probably underestimated. In the course of this presentation, we deliberately restricted discussion to issues raised in recent years concerning the extent of this syndrome. We discuss diagnostic criteria, especially electrophysiological ones. As the criteria proposed by the ad hoc committee of the American Academy of Neurology in 1991 have been questioned due to lack of sensitivity, new ones have been proposed recently. We briefly discuss the different types of chronic dysimmune demyelinating neuropathy: not only the CIDP, but also the Lewis and Sumner syndrome or multifocal inflammatory demyelinating neuropathy and the multiple conduction block neuropathies. At last, we point out the consistent finding of axonal involvement in the course of a chronic demyelinating neuropathy; over time, it can become predominant, which may make diagnosis difficult by suggesting a chronic axonal neuropathy that may be assumed to be primary. Consideration of these points may help clinicians recognize more chronic dysimmune neuropathies, for which immunosuppressive therapy has been found to be effective.

Journal Article↗
PubMed2002

Anti-glycolipid antibodies in the diagnosis of autoimmune neuropathies.

Recent years have seen major progress in our understanding of the clinical pathophysiology of autoimmune neuropathies particularly with the identification and analysis of antibodies to gangliosides and related glycolipids in the serum of patients. Anti-glycolipid antibodies react with epitopes on the carbohydrate region of glycolipid molecules and can be routinely measured by standard immunoassays. In multifocal motor neuropathy, IgM anti-GM1 antibodies that cross react with GD1b and asialo-GM1 are detectable in around 50p. 100 of cases. This condition may clinically resemble certain forms of lower motor neurone disease. IgM anti-GD1b antibodies are found in IgM paraproteinaemic neuropathy characterised by profound sensory ataxia. In the anti-myelin associated glycoprotein (anti-MAG) IgM paraproteinaemic neuropathy, antibodies also react with the acidic glycolipids, sulphated glucuronyl paragloboside and its higher lactosaminyl homologue (SGPG and SGPLG). Thus a variety of chronic syndromes can be defined by their anti-glycolipid antibody profile. In Guillain-Barré syndrome, anti GM1, GM1b, GD1a and GalNAc-GD1a antibodies are found in patients with acute motor axonal neuropathy (AMAN) and anti-GQ1b IgG antibodies are a very sensitive and specific marker for the Miller Fisher syndrome. Many other anti-glycolipid antibodies are being increasingly identified in other neuropathy subtypes. The article will summarise existing clinical and serological information in this field.

Acute Disease↗
PubMed2003

Peripheral neuropathy associated with treatment for multidrug-resistant tuberculosis.

OBJECTIVE: To review the incidence and management of peripheral neuropathy in patients receiving therapy for MDR-TB. METHODS: A case series with retrospective chart review of 75 patients who initiated individualized therapy for multidrug-resistant tuberculosis (MDR-TB) in Lima, Peru, between 1 August 1996 and 31 January 1999. RESULTS: All patients had confirmed MDR-TB and were receiving individualized therapy, comprised of an average of six drugs. Ten (13%) of these patients presented with symptoms of peripheral neuropathy, confirmed by electromyography. All symptoms were reported in the lower extremities, and all were sensory in nature. Median time to presentation from initiation of MDR-TB therapy was 9.1 months. No significant risk factors associated with development of peripheral neuropathy were identified. Management strategies depended on the severity of symptoms and included the treatment of contributing co-morbidities, medications for neuropathic pain, and adjustment of doses of possible offending agents. All patients responded to management; three patients were left with mild residual symptoms. Patients whose neuropathy resolved had symptoms for a median of 7 months. CONCLUSIONS: Peripheral neuropathy was encountered in 13% of our cohort of MDR-TB patients. The diagnosis of peripheral neuropathy can be based on clinical presentation alone, and effective management of this side-effect is possible without sacrificing MDR-TB treatment efficacy.

Adolescent↗
PubMed2003

[Molecular mechanisms of hereditary neuropathy: genotype-phenotype correlation].

Hereditary neuropathies are classified into several subtypes according to clinical, electrophysiologic and pathologic findings. Recent genetic studies have revealed their phenotypic and genetic diversities. In the primary peripheral demyelinating neuropathies(CMT1), at least 9 genes have been associated with the disorders; altered dosage of peripheral myelin protein 22(PMP22) or point mutation of PMP22, the gap junction protein 1(GJB1), the myelin protein zero gene(MPZ), the early growth response gene 2(EGR2), the myotubularin-related protein 2 gene(MTMR2), the N-myc downstream-regulated gene 1 (NDRG1), the L-periaxin gene(PRX), SRY-related HMG-BOX gene 10(SOX10) and the ganglioside-induced differentiation-associated protein 1 gene(GDAP1). In the primary peripheral axonal neuropathies(CMT2), at least 8 genes have been associated with these disorders; the neurofilament light chain gene(NEFL), the kinesin 1B gene(KIF1B), the gigaxonin gene(GAN1), Lamin A/C(LMNA) and tyrosyl-DNA phosphodiesterase 1(TDP1). In addition, some mutations in GJB1, MPZ and GDAP1 also present with clinical and electrophysiologic findings of CMT2. Mutation of NEFL or KIF1B cause dominantly inherited axonal neuropathies, whereas mutation of GJB1 or MPZ can present as genocopies of dominant axonal neuropathies. In addition to the above diseases, we have reported a new type of NMSNP(MIM # *604484) characterized by proximal dominant neurogenic atrophy, obvious sensory nerve involvement and the gene locus on 3q13. Here, we summarize the genetic bases of hereditary neuropathies and attempt to highlight significant genotype-phenotype correlations.

Axons↗
PubMed2003

[The painful multiple mononeuropathy of acute onset in the left arm which was diagnosed as leprous neuropathy].

A 31-year-old man from Myanmar with leprous neuropathy was reported. The progress of the disease was subacute but the painful symptom at the time of the onset was acute. Multiple mononeuropathy was diagnosed by the biopsy findings of the left superficial radial nerve. He was admitted to our hospital with the complaint of the weakness of his left hand and fingers which were very painful and got worse in several weeks. Motor palsy was observed in his left ulnar, median, and radial nerves, and there was the hypesthesia or anesthesia in his left hand, forearm and the medial side of his left upper arm. On nerve conduction studies, the amplitudes of CMAP and SNAP severely diminished or not detected. The pattern was compatible with multiple mononeuropathy. The biopsy of the left superficial radial nerve was performed. The pathological findings were the destruction of nerve fascicles, replacement of nerve fibers with inflammatory cells, and Mycobacterium leprae was found with the specific stain. These findings confirmed the diagnosis of the leprous neuropathy. Leprous neuropathy is one of the commonest causes of infectious neuropathy in the world, especially in Southeast Asia. These days many foreign workers from that area are staying in Japan, and the chances to see the disease are increasing. We have to recognize leprous neuropathy as a candidate for the multiple mononeuropathy of acute onset with painful dysesthesia similar to vascular neuropathy.

Acute Disease↗