scholarly journals Subacute Spinal Subdural Hematoma in One-Year Old Boy Due to Severe Hemophilia A

2021 ◽  
Vol 7 (3) ◽  
pp. 134-137
Author(s):  
Tun Paksi Sareharto ◽  
Suciati Jandraningrum ◽  
Vetty Kurniawati ◽  
Agus Priambodo ◽  
Alifiani Hikmah Putranti
Keyword(s):  
Spinal Cord ◽  
Physical Examination ◽  
Factor Viii ◽  
Motor Neuron ◽  
Subdural Hematoma ◽  
Rare Case ◽  
Hemophilia A ◽  
Lower Motor Neuron ◽  
Increased Risk ◽  
Spinal Subdural Hematoma

Background: Paraparesis may result from a variety of or primary central nervous system conditions or systemic disorders, and although rare, it may also caused by spinal cord hemorrhage. Spontaneous spinal subdural hematomas (SSDH) are most frequently associated with coagulopathies. People with congenital clotting disorders such as hemophilia are at increased risk for experiencing spontaneous spinal subdural hemorrhage at unusual sites, which is a rare case and a neurological emergency required urgent recognition. We report a boy with paraparesis caused by subacute SSDH due to hemophilia A. Case Presentation: A 15 month-old boy, with chief complain of difficulty in moving his leg and pain when walking, physical examination revealed a lower motor neuron lesion, laboratory showed a low factor VIII at 0.4% level, Magnetic Resonance Imaging (MRI) showed anterior and posterior displacement of the spinal cord due to the presence of the subacute subdural hematoma extending from 1st cervical to 1st lumbar spine. He assessed with inferior paraparesis caused by subacute spinal subdural hematoma due to hemophilia A. The patient’s condition was improved after received replacement therapy of factor VIII and proper laminectomy neurosurgery. Conclusion: This case showed an approach for a comprehensive diagnostic and management for a rare case of paraparesis due to hemophilia. Pay attention to the physical examination which shows a lower motor neuron lesion in an acute paralysis cases, there is still a possibility that it is an upper motor neuron lesion. 

scholarly journals Spinal Subdural Hematoma in Association with Anticoagulant Therapy

1981 ◽  
Vol 8 (1) ◽  
pp. 87-89 ◽  
Author(s):  
Neville Russell ◽  
F.B. Maroun ◽  
J.C. Jacob
Keyword(s):  
Spinal Cord ◽  
Clinical Features ◽  
Anticoagulant Therapy ◽  
Spinal Cord Compression ◽  
Subdural Hematoma ◽  
Cord Compression ◽  
Ischemic Necrosis ◽  
Results Of Treatment ◽  
Spinal Subdural Hematoma

SUMMARYA case of spinal subdural hematoma occurring in association with anticoagulant therapy is reported. Seven similar cases from the literature are reviewed with emphasis on the clinical features, investigation, and the results of treatment. The prognosis for recovery is good, only if the condition is diagnosed and the clot evacuated before severe spinal cord compression and subsequent ischemic necrosis has occurred.

Tubercular longitudinally extensive transverse myelitis with lower motor neuron paralysis

2020 ◽  
pp. 004947552095644
Author(s):  
Manjeet Kumar Goyal ◽  
Mahesh Lal
Keyword(s):  
Spinal Cord ◽  
Motor Neuron ◽  
Spinal Tuberculosis ◽  
Transverse Myelitis ◽  
Lower Motor Neuron ◽  
Neuron Type ◽  
Longitudinally Extensive Transverse Myelitis ◽  
Longitudinal Extensive Transverse Myelitis ◽  
Spinal Segments ◽  
Extensive Transverse Myelitis

Transverse myelitis typically extends two or less spinal segments, whereas longitudinal extensive transverse myelitis (LETM) extends three or more spinal segments in length and may occasionally span all the segments of the spinal cord. We present a case of spinal tuberculosis presenting with LETM with true lower motor neuron-type flaccid paraplegia.

Lower Motor Neuron Disease with Accumulation of Neurofilaments in a Cat

1976 ◽  
Vol 13 (6) ◽  
pp. 428-435 ◽  
Author(s):  
M. Vandevelde ◽  
C. E. Greene ◽  
E. J. Hoff
Keyword(s):  
Spinal Cord ◽  
Motor Neuron ◽  
Motor Neuron Disease ◽  
Histological Examination ◽  
Muscle Atrophy ◽  
Motor Neurons ◽  
Nerve Cells ◽  
Lower Motor Neuron ◽  
Motor Neuron Diseases ◽  
Lower Motor Neuron Disease

A young cat had signs of tetraparesis that progressed to tetraplegia within a few weeks. Clinically, there was lower motor neuron disease with areflexia and muscle atrophy in all limbs. Degeneration of the motor neurons in the spinal cord was seen on histological examination. Ultrastructurally, the degeneration of nerve cells was characterized by abnormal proliferation of neurofilaments. These findings were compared to other motor neuron diseases and neurofibrillary accumulations in man and animals.

scholarly journals Lower Motor Neuron Syndrome Following Radiotherapy

1983 ◽  
Vol 10 (1) ◽  
pp. 56-58 ◽  
Author(s):  
Sandra L. Horowitz ◽  
John D. Stewart
Keyword(s):  
Spinal Cord ◽  
Motor Neuron ◽  
Anterior Horn ◽  
Lower Motor Neuron ◽  
Lower Abdomen ◽  
Post Irradiation ◽  
Leg Weakness ◽  
Muscle Biopsies ◽  
Sacral Radiculopathy ◽  
Motor Neuron Syndrome

SUMMARY:A 33 year old man developed bilateral leg weakness two years following radiotherapy to the pelvis and lower abdomen for the treatment of a seminoma. Clinical and electrophysiological examinations and nerve and muscle biopsies suggest that this is an example of either post-irradiation myelopathy selectively affecting the anterior horn cells in the lower spinal cord or a purely motor lumbo-sacral radiculopathy.

scholarly journals Giant Subgaleal cerebrospinal fluid leakage: An unusual complication of chronic subdural hematoma surgery

2017 ◽  
Vol 31 (3) ◽  
pp. 316-318
Author(s):  
Luis Rafael Moscote-Salazar ◽  
Hernando Raphael Alvis-Miranda ◽  
Amit Agrawal ◽  
Willem Calderon-Miranda ◽  
Alfonso Pacheco-Hernandez
Keyword(s):  
Cerebrospinal Fluid ◽  
Physical Examination ◽  
Mental Status ◽  
Subdural Hematoma ◽  
Neurological Disorder ◽  
Rare Case ◽  
Chronic Subdural Hematoma ◽  
Cerebrospinal Fluid Leakage ◽  
Unusual Complication ◽  
Fluid Leakage

Abstract We report a rare case of chronic subdural hematoma complicated with a Giant subgaleal cerebrospinal fluid leakage. Physical examination was performed with no alteration in mental status and no focal neurological disorder. The subdural hematoma was drained and two weeks later, patient was admitted to our hospital with a giant scalp swelling. Physical examination revealed a left parietal subcutaneous collection. The patient was reoperated with a correction in the fistula, he presented a satisfactory postoperative evolution. To our knowledge, this is the first report in literature of a chronic subdural hematoma with a complicated giant subgaleal cerebrospinal fluid leakage.

Incidence of Factor VIII Inhibitor Development in Hemophilia A Patients Treated with Less Pure Plasma Derived Concentrates

1994 ◽  
Vol 71 (05) ◽  
pp. 544-547 ◽  
Author(s):  
R de Biasi ◽  
A Rocino ◽  
M L Papa ◽  
E Salerno ◽  
L Mastrullo ◽  
...  
Keyword(s):  
Factor Viii ◽  
High Purity ◽  
Hemophilia A ◽  
Cumulative Risk ◽  
Factor Viii Inhibitor ◽  
Anamnestic Response ◽  
Inhibitor Development ◽  
Increased Risk ◽  
Factor Viii Concentrates ◽  
Very High

SummaryVery-high-purity Factor VIII concentrates produced by monoclonal or recombinant technology have been postulated to be more antigenic resulting in an increased risk of inhibitor development in hemophilia A patients. However, previous reports, mainly based on prevalence figures, may have understimated the “true” risk of this complication in patients treated with less pure Factor VIII concentrates. The present study, started in 1975, has been designed to calculate the risk of inhibitor development in patients with severe or moderate hemophilia A, followed since their first exposure to intermediate or high-purity Factor VIII concentrates, produced by conventional technologies. Sixty-four hemophiliacs fulfilled the enrollment criteria. Inhibitors developed in 20.3% (13/64) of all patients and in 23% (11/48) of those with severe Factor VIII deficiency. Eleven patients manifested a strong anamnestic response after exposure to Factor VIII (high responders) and 2 had low inhibitor concenlialions despite repeated Factor Vlll infusions (low responders). The incidence of inhibitor development was 24.6 per 1000 patient yeuis of observalion. The, cumulative! risk of inhibitor formation was 19,9% at age of 6 years, and 20.3% at 5 years after the first exposure. The risk was 19.3% at 70 days of exposure to Factor VIII concentrates, and 17.2% after a total of 50,000 units of Factor VIII given.Further stuides are needed to confirm the above risk of acquiring an inhibitor, which indicates and under-estimations by previous studies. In addition, more data is needed to demonstrate whether very high purity Factor VIII concentrates may be more antigenie than conventional preparations.

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