DEGENERACION SUBAGUDA COMBINADA PDF

DEGENERACION SUBAGUDA COMBINADA PDF

MRI of spinal cord and brain lesions in subacute combined degeneration. Degeneracion subaguda combinada secundaria a infeccion cronica por Helicobacter. Cornejo W, Gonzalez F, Toro ME, Cabrera D. Degeneracion combinada subaguda. Descripcion de un caso en un nino vegetariano estricto. Rev. Neurol. Cornejo W, Gonzalez F, Toro ME, Cabrera D. Degeneracion combinada subaguda. Descripcion de un caso en un nino vegetariano estricto. Rev Neurol.

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Subacute combined degeneration is an acquired myelopathy caused by vitamin B12 deficiency. Therapy with B12 leads to improvement in most but to complete recovery in only a combinara patients.

Prognostic indicators in subacute combined degeneration are unknown; therefore, predicting complete recovery of neurologic deficits is challenging.

To identify potential correlates of outcome and to generate hypotheses concerning predictors of complete resolution of neurologic deficits in subacute combined degeneration.

Reports of patients with subacute combined degeneration containing degeneravion of magnetic resonance imaging MRI and description of outcome and 1 patient degeeracion by the authors. We extracted data from 45 reports and 57 patients 36 males, 21 females; age range: The absence of sensory dermatomal deficit, Romberg, and Babinski signs were associated with a higher complete resolution rate.

B12 therapy is reported to stop progression and improve neurologic deficits in most patients with subacute combined degeneration. However, complete resolution only occurs in a small percentage of patients and appears to be associated with factors suggestive of less severe disease at the time of diagnosis.

Combiada B12 deficiency can lead to serious neurologic complications including peripheral neuropathy, bilateral cerebral dysfunction, optic neuropathy, memory loss, personality changes, impaired recall, and subacute combined degeneration of the spinal cord.

Degeneració subaguda combinada de la medul·la espinal – Viquipèdia, l’enciclopèdia lliure

It is surprising, however, that despite improvement in diagnostic tools, such as magnetic resonance imaging MRIand effective therapy, data on prognostic indicators and predictors of complete resolution of neurologic deficits in subacute combined degeneration are sorely lacking. When treating eubaguda disease, physicians are unable to predict whether a patient will have complete resolution or only improvement of the disabling neurologic deficits. Therefore, in this study, we sought to identify clinical, laboratory, and radiological factors present at the time of diagnosis that could potentially correlate with resolution of neurologic deficits in patients with subacute combined degeneration.

Combinda also included data from a patient treated by the authors. We selected combinads of patients with 16 subacute combined degeneration that described results of MRI and patient’s outcome after B12 therapy.

We included patients who met edgeneracion following criteria Patients with preexistent or concomitant neurologic pathology multiple sclerosis, tumors described in the history or suggested by MRI were excluded. We extracted demographic, clinical, laboratory, and radiologic data. Potential predictive factors variable and outcome complete resolution or improvement only were reviewed independently by 2 neurologists O. Discrepancies between data fields occurred in 2 instances and were related to reports written in a foreign language.

These discrepancies were addressed with a translator and joint review of the manuscripts. As all reports identified in the literature only described patients who improved with B12 therapy, clinical outcomes were defined as improvement arrest subagudq disease progression followed by improvement but persistence of neurologic deficits or complete resolution arrest of disease progression followed by complete resolution of neurologic deficits.

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We evaluated the quality of the reports by assessing the accuracy of diagnosis, appropriateness of therapy, and report of clinical, laboratory, and radiological variables, and clinical outcome. Data combknada 57 patients were used to estimate the strength of association between 18 clinical, laboratory, and radiologic factors Table 1 and resolution of signs and symptoms in patients with subacute combined degeneration.

The strength of the association is indicated by the magnitude of the difference in complete resolution rates between patients with and without a given factor.

Statistical analyses were conducted using MIX version 1. We identified potentially relevant reports and eliminated lacking case studies, confirmed diagnosis, patient outcome, or MRI data.

Although we searched the literature sincethe earliest report containing MRI data was from A year-old male developed paresthesias and gait disturbance after general anesthesia including nitrous oxide.

Symptoms and signs included leg weakness, erectile dysfunction, impaired bowel and bladder control, spastic quadriparesis, diffuse hypereflexia, extensor plantar responses, ataxic-paretic gait, Romberg sign, proprioceptive and vibratory sensory loss in the legs, and sensory deficit to T5. Laboratory studies showed macrocytic anemia and low serum B Spine MRI showed increased T2-weighted signal intensity of posterior columns and low T1-weighted signal intensity in the bone marrow Fig.

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Admission sagittal A and axial B spine MR sequences of a year-old male showing an increased T2-weighted cord signal involving the posterior columns. Follow-up scan obtained 4 months after initiation of therapy showing significant resolution of the signal changes, correlating with clinical improvement C deeneracion D.

T1-weighted sequences on admission revealed a low signal in the bone marrow of the vertebral bodies E. Rescue of bone marrow signal intensity was seen after 4 months of therapy F. The mean age of patients who had complete resolution of signs and usbaguda after B12 therapy was The median duration of illness at the time of diagnosis was 6 weeks range 2 to 24 weeks in patients who had complete resolution and 12 range 1 to 84 weeks in patients who only had improvement with B12 therapy.

Only 1 patient had no reported risk factor for B12 subagudz. In 15 patients, exposure to nitrous oxide preceded the development of subacute combined degeneration during surgical cmbinada or chronic recreational use. Reported signs and symptoms included symmetric ascending paresthesias, sensory loss, muscle weakness, ataxia, and gait abnormalities. Sensory degeneraion in a stocking glove distribution pattern and sharp spinal level from C2 to Subagda were reported.

Tendon reflex abnormalities were ubiquitous and ranged from generalized hypereflexia with clonus to absent reflexes. Dissociation between upper hyperactive and lower decreased or absent extremity reflexes was reported frequently. In lower limbs, coexistence of hyperactive knee responses and hypoactive or absent ankle jerks was commonly observed.

Sphincter dysfunction was present in a few patients. On MRI, several patterns were described: Increased T2-weighted signal intensity in dorsal columns was the most common finding. After initiation of B12 therapy, all patients reported in the literature showed, at a minimum, arrest of progression of neurologic deficits.

Resolution of radiological abnormalities on follow-up scans occurred in 5 of 8 subjects who had complete resolution of deficits. Conversely, in a few patients, follow-up MRI normalized despite persistence of neurologic deficits paresthesias and sensory loss.

In 2 subjects, clinical resolution preceded normalization of spine MRI findings. In these 2 cases, follow-up scan was obtained 12 to 24 weeks after the first study. In 2 subjects with segmental atrophy of the thoracic spinal cord, B12 therapy led to symptomatic improvement but no appreciable functional gain. Possible correlates of outcome in patients with subacute combined degeneration and their respective magnitude of association are shown in Table 1.

As indicated by the magnitude of differences in clinical resolution rates, factors showing a strong association with complete resolution of signs and symptoms include absence of sensory level, Romberg and Babinski sign, and spinal cord atrophy.

While several medical specialties are likely to evaluate patients with subacute combined degeneration, little information on predictors of outcome is available. However, the fact that we found no reports of patients with subacute combined degeneration who failed to improve after therapy limits our conclusions to only those patients who respond to B12 therapy.

We acknowledge that patients who do not respond to therapy, and have not been reported in the literature, may have similar characteristics. Our findings suggest that absence of sensory level, Romberg and Babinski signs may be associated with clinical resolution of signs and symptoms in patients with subacute combined degeneration.

It is known that the presence of sensory level reflects spinal cord damage that interrupts transmission of sensory impulses to higher centers in the central nervous system, Romberg sign reflects blockade of deep sensory impulses from lower extremities and severe compromise of heavily myelinated sensory axons along the posterior columns, and that Babinski sign reflects damage to corticospinal tract fibers traveling in the lateral funiculi of the spinal cord.

Therefore, it is conceivable that patients without sensory level, Romberg, and Babinski signs have less severe disease and therefore a higher likelihood of achieving complete resolution of neurologic deficits with B12 therapy. This is not surprising as younger patients have greater nervous system plasticity.

The report of a year-old who recovered despite extensive spinal cord involvement further supports this hypothesis.

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Therefore, our findings support the notion that younger age and, as previously combinafa by others, 3 shorter duration of illness positively impact on the likelihood of reaching complete resolution with B12 in subacute combined degeneration.

The reports indicate that subacute combined degeneration is associated with heterogeneous patterns on MRI, suggesting that the disease may be a degendracion areas of demyelination gradually coalesce into larger spinal cord lesions as described in neuropathologic studies.

These findings support the notion that patients with less severe spinal cord involvement on MRI are likely to have less severe disease and therefore higher resolution rates after B12 treatment. Another interesting observation was that in a few patients, resolution of clinical signs and symptoms preceded normalization of MRI abnormalities. This suggests that, in the absence of axonal injury, clinical resolution after B12 may precede normalization of increased T2-weighted signal on MRI, which reflects edema of myelin sheaths.

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Overall, our study raises the possibility that MRI findings at the time of diagnosis combinzda be potential correlates of outcome and have a prognostic value in subacute combined degeneration.

While the majority of patients in our study had pernicious anemia, our findings suggest that the absence of anemia was associated with higher rates of resolution of neurologic deficits after B12 therapy. This finding was surprising as the severity of comibnada changes in subjects with pernicious anemia does not appear to correlate with neurological complications. In addition, all patients reported with subacute combined degeneration had some improvement with B12 therapy despite variability of regimens.

These findings, along with MRI and the clinical factors described above, suggest that lesser disease severity and duration, rather than etiology, is associated with degeneracin resolution of signs and symptoms of subacute combined degeneration.

Of interest, 15 of 57 patients included in this study developed subacute combine degeneration after exposure to nitrous oxide either during a general anesthetic or after chronic use as a recreational drug. It is known that nitrous oxide affects vitamin B12 metabolism by oxidizing its reduced form.

In turn, as the reduced form of B12, a coenzyme for methionine synthase, is oxidized, methionine synthase is inhibited by deprivation of the reduced form of B Consequently, the transmethylation of homocysteine to degeneracin catalyzed by methionine synthase is impaired, which in turn can ultimately impact on DNA, myelin, and catecholamine synthesis. In addition, in patients with newly diagnosed myelopathy, the possibility of nitrous oxide abuse should be explored as cessation of exposure subaguad necessary for successful therapy.

Although our study generates valuable information that should be further evaluated in future studies, it has limitations. Subaguds include its retrospective nature, uncontrollable variability of diagnostic criteria and treatment regimens, number of treating centers, and lack of standardized tools to measure outcomes and standard follow-ups. While informative and the first to suggest that clinical and radiological findings at the time of diagnosis can potentially correlate with resolution of neurologic deficits, our study simply generates hypotheses about the biology of subacute combined degeneration that warrant degenerafion testing.

Nevertheless, our findings suggest that young patients with less severe neurologic comvinada, less extensive spinal cord lesions on MRI, who are treated earlier in the course of the disease, are likely to have higher resolution rates of signs and symptoms caused by subacute combined degeneration.

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subacute combined degeneration

J Gen Intern Med. Author information Article notes Copyright and License information Disclaimer. The authors have no conflicts of interest to report. The opinions or assertions contained herein are the private views of the authors and are not to be construed as official or as reflecting the views of the Department of the Army or the Department of Defense.

Address correspondence and requests for reprints to Dr. This article has been cited by other articles in PMC. PURPOSE To identify potential correlates of outcome and to generate hypotheses concerning predictors of complete resolution of neurologic deficits in subacute combined degeneration.

Reports Selection We selected reports of patients with 16 subacute combined degeneration that described results of MRI and patient’s outcome after B12 therapy. Data Extraction We extracted demographic, clinical, laboratory, and radiologic data. Data Synthesis and Analysis Data from 57 patients were used to estimate the strength of association between 18 clinical, laboratory, and radiologic factors Table 1 and resolution of signs and symptoms in patients with subacute combined degeneration.

Open in a separate window. Anemia was defined as a hemoglobin level below and macrocytosis as a mean corpuscular volume above the normal reference range of the reporting institution. The strength of association between a given finding and complete clinical resolution is indicated by the magnitude of the difference in complete resolution rates between patients with and without a given factor.

Patient Treated by the Authors A year-old male developed paresthesias and gait disturbance after general anesthesia including nitrous oxide.

Clinical, Laboratory, and Radiologic Profile The mean age of patients who had complete resolution of signs and symptoms after B12 therapy was