Paraparesis after Spinal Anesthesia During Delivery.

Traumatic injury to the spinal cord during spinal or epidural anesthesia is usually secondary to either direct needle penetration or intra-neural injection of local anesthetics. Two women were admitted to a rehabilitation department with paraparesis and hypoesthesia after delivery. One had undergone a lower segment cesarean section under spinal anesthesia and the other, a spontaneous delivery under epidural anesthesia. After discharge from the rehabilitation treatment, they both experienced some weakness in the lower limbs. The patho-physiological basis of this complication seems to be either direct damage to the spinal cord by intra-neural injection of local anesthetics, or local ischemia.

Complete clinical and functional recovery following low-dose methotrexate related paraparesis in a patient with compound c.1298A>C AND c.677C>T MTHFR polymorphism: A case report.

RATIONALE: The mechanisms of action of MTX (methotrexate) in the treatment of RA (rheumatoid arthritis) and PsA (psoriatic arthritis) is related to its antifolic activity, due to the high affinity for enzymes that require folate cofactors as dihydrofolate reductase and to the anti-inflammatory activity derivated from the inhibition of thymidylate synthetase that leads to the over-production of adenosine. PATIENT CONCERNS: Our patient was a 41-year-old female, affected by PsA in treatment since 2 years with low-dose methylprednisolone and low-dose subcutaneous MTX. The treatment was effective. The patient subacutely developed a severe paraparesis with impossibility of gait or standing without aid and was admitted to a Neurology Department where the cause of the paraparesis was not clear in spite of accurate radiological neurophysiologic and laboratory tests. Therefore, she was admitted in a rehabilitation unit. DIAGNOSIS AND INTERVENTIONS: Paraparesis in PsA patient in treatment with methotrexate. MTX toxicity was hypothesized; therefore the drug was discontinued while i.m. folic acid and cyanocobalamin were administered for 20 days. The diagnosis was clinical, based on neurological examination (paraparesis) and on the chronic use of MTX (hypothesis of toxicity). OUTCOMES: The patient obtained a complete resolution of paraparesis. Genetic analyses showed associated a compound heterozygosity for the c.1298A>C and c.677C>T variants of methylenetetrahydrofolate reductase (MTHFR) gene. LESSONS: Neurological side effects of MTX are uncommon. In literature no previous case of MTX induced paraparesis in patients treated with low-dose MTX for chronic arthritis has been described. The association between the gene polymorphisms of MTHFR (c.1298A>C and c.677C>T) and MTX toxicity in arthritis patients is confirmed. The case also confirms that folates are a precious antidote of MTX toxicity.

ANIMAL TRAINING AND ACUPUNCTURE IN A BENGAL TIGER ( PANTHERA TIGRIS TIGRIS) WITH HIND LIMB PARAPARESIS.

An 18-yr-old, captive-born male Bengal tiger ( Panthera tigris tigris) presented a 1-yr history of chronic and progressive paraparesis in both hind limbs. Lateral and hind limb radiographs were revealed normal except for severe spondylosis deformans, forming a bony bridge between the last lumbar and the first sacral vertebra and disc mineralization between the second and third lumbar vertebra. Medical therapies were instituted, including corticosteroids, hydroacupuncture and electroacupuncture. Animal training allowed veterinarians to perform acupuncture safely without having to anesthetize the animal. Animal training made intensive treatment possible. Neither corticosteroids nor hydroacupuncture alone provided much clinical improvement. The tiger reacted positively after electroacupuncture was performed. The tiger began showing clinical improvement after three electroacupuncture treatments and could eventually walk on all four limbs at the end of the treatment.

Hereditary ataxias and paraparesias: clinical and genetic update.

PURPOSE OF REVIEW: This review aims at updating the clinical and genetic aspects of hereditary spastic paraplegias (HSPs) and hereditary cerebellar ataxias (HCAs), focusing on the concept of spastic-ataxia phenotypic spectrum and on newly identified clinical overlaps with other neurological and nonneurological diseases. RECENT FINDINGS: Next-generation sequencing (NGS) has allowed the discovery of new genes involved in HSPs and HCAs. They include new HCAs genes such as GRM1 (SCA44), FAT2 (SCA45), PLD3 (SCA46), SCYL1 (SCAR21), UBA5 (SCAR24) and XRCC1 (SCAR26) as well as CAPN1 (SPG76) and CPT1C (SPG73) in HSPs. Furthermore, NGS allowed enriching known genes phenotype, reinforcing the overlap between HSPs and HCAs defining the spastic ataxia spectrum. Clear examples are the expanded phenotypes associated with mutations in SPG7, PNPLA6, GBA2, KIF1C, CYP7B1, FA2H, ATP13A2 and many others. Moreover, other genes not previously linked to HCAs and HSPs have been implicated in spastic or ataxic phenotypes. SUMMARY: The increase of HSPs and HCAs-related phenotypes and the continuous discovery of genes complicate clinical diagnostic in practice but, at the same time, it helps highlighting common pathological pathways, therefore opening new ways to the development of common therapeutic approaches.

Delayed onset paraparesis complicating epidural steroid injection with underlying spinal dural arteriovenous fistula.

We report a case of a 48-year-old man with chronic back pain attributed to discogenic lumbar radiculopathy who underwent a fluoroscopy-guided L2-3 interlaminar epidural steroid injection. 4 h later, he developed acute paraparesis, sensory loss below T10 level and urinary retention. MRI of the thoracic spine revealed diffuse abnormal T2/FLAIR signal and extensive vascular flow voids. A spinal dural arteriovenous fistula was confirmed on spinal angiography. Embolization of the spinal dural arteriovenous fistula resulted in significant improvement of symptoms. We review previously reported cases and current understanding of the pathophysiology of this complication. All cases had symptom onset several hours after the procedure. There seems to be a trend toward better outcomes with earlier treatment.

Thoracic Hemangioma From Rib Presenting as Compressive Paraparesis in a Young Adult: A Treatment Dilemma.

STUDY DESIGN: A case report. OBJECTIVE: To describe the presentation of compressive paraparesis as a result of thoracic rib hemangioma in a young adult and its nonsurgical management. SUMMARY OF BACKGROUND DATA: Hemangiomas are rare bone tumors and those arising from rib are rarer. Only about 50 such cases have been reported in literature so far. METHODS: A 21-year-old male student, presented to us with a 6-week history of progressive weakness in both lower limbs and loss of bowel bladder control. Patient gave history of being operated for left periscapular tumor treated with wide excision and proven with biopsy to be a hemangioendothelioma (benign but locally aggressive hemangioma variant) a year ago. RESULTS: New radiograph of the chest showed an expansile lesion of left fifth rib and magnetic resonance image showed a tumor of left dorsal thoracic wall with AV malformation causing compressive thoracic myelopathy at T5 level vertebrae. We planned for immediate decompression surgery for spine along with excision of tumor with the help of a thoracic surgeon. However, on preoperative digital subtraction angiography, the tumor was found to be highly vascular with high risk of intraoperative bleeding and morbidity. So, the plan was revised and the patient underwent digital subtraction angiography, followed by embolization by an expert interventional neurosurgeon. The patient showed signs of recovery within a week. Lower limb power improved from grade 2 to 3/5 to grade 4 to 4+/5. The patient became ambulatory with single stick at 3-month follow-up; he was a nonwalker to start with. At 2 years plus follow-up, the patient fully recovered and walks without stick. CONCLUSION: This unique case brings to light the dilemma a spine surgeon sometimes faces. A case that warranted immediate surgical intervention based on clinical findings was treated with interventional fibrin glue embolizations with excellent results. LEVEL OF EVIDENCE: N/A.

Neurological deterioration induced by sitting in patients after cervicothoracic posterior decompression with instrumented fusion surgery for ossification of the longitudinal ligament: two cases reports.

BACKGROUND: We report on Japanese patients who showed neurological deterioration induced by sitting after cervicothoracic posterior decompression with instrumented fusion, but showed immediate neurological recovery after bed rest. CASE PRESENTATION: Patients showed incomplete paraparesis caused by the ossification of the posterior longitudinal ligament at uppermost thoracic spine. Cervicothoracic posterior decompression with instrumented fusion was performed. Postoperatively, the patients showed partial paraparesis when they were sitting. They showed rapid recovery from lower extremity paralysis upon lying down. After strict bed rest for one month, those patients showed no apparent development of paralysis during sitting. CONCLUSION: In patients with postoperative residual anterior spinal cord compression, micromotion might exacerbate neurological symptoms.

Teaching case: a man with a progressive gait impairment and visual compromise.

Primary progressive multiple sclerosis can present with a wide variety of symptoms. We report a case of a 52-year-old man presenting with visual symptoms and gait impairment in whom a diagnosis of a primary progressive multiple sclerosis was established. Symptomatic treatment with dalfampridine was started but did not result in a considerable improvement. Gait disorders in multiple sclerosis are common and can have a considerable effect over the patient׳s quality of life. Dalfampridine is the first drug approved for the symptomatic treatment of gait in MS, although only a 40% of patients show an objective response to this medication. Primary progressive multiple sclerosis represents a therapeutic challenge. Currently, there are no disease modifying treatments approved but there are several medications undergoing assessment for this indication. Further research in the underlying pathophysiology of PPMS will help us develope more successful disease-modifying treatments. Meanwhile, a symptomatic approach should be offered in order to improve the patient׳s quality of life.

Hernia diafragmática traumática derecha / Right traumatic diaphragmatic hernia

Paciente masculino, de 47 años de edad que sufrió un accidente automovilístico en el año 1991, con fractura de columna lumbar , que dejó como secuela una paraparesia flácida postraumática con nivel neurológico de lesión del segmento L5, con disminución de la fuerza muscular y de la sensibilidad en las extremidades inferiores. Se le hizo inmovilización con yeso durante 6 meses y fue intervenido quirúrgicamente en ese propio año. Se le realizó fijación y osteosíntesis con material metálico. Se rehabilitó durante varios anos alcanzando buen fortalecimiento muscular y en noviembre de 2008, en horas de la noche, comienza con dolor intenso a nivel de hipocondrio y hemitórax derecho, que se incrementa con el decúbito supino y mejora con el decúbito lateral izquierdo y con disnea moderada. Al examen físico del tórax, se constató aumento de la matidez del tercio inferior del hemitórax derecho y se auscultaron ruidos hidroaéreos a este nivel. Se realizó radiografía (Rx) de tórax vista posteroanterior(PA), donde se constató elevación del hemidiafragma derecho e imagen compatible con presencia de asas intestinales en el tercio inferior de este hemitórax. Se diagnosticó una hernia diafragmática traumática derecha , que es una enfermedad poco frecuente debido al efecto amortiguador del hígado. Se realizó tratamiento médico inicialmente y una hora después , cesa el dolor. Se redujo la hernia de manera espontánea, lo que se corroboró en el Rx de tórax ( vista PA) evolutivo. Posteriormente fue intervenido quirúrgicamente de forma electiva y el resultado fue favorable(AU)

A 47 years-old male patient, who was injured in a car accident in 1991 and suffered lumbar column fracture that left as a sequel a postraumatic flaccid paraparesia with neurological lesion of L5 segment, reduction of muscle strength and sensitivity in lower limbs. He had plaster for 6 months and was surgically treated in that year. He underwent fixation and osteosynthesis with metal material. During several years, he went to rehabilitation program and finally achieved good muscle strengthening. In November 2008, he began feeling intense pain at hypochondrium and right hemithorax at night and also moderate dyspnea. On the physical exam, it was confirmed that there was increase of lower third of right hemithorax and hydroaerial noises were heard. Chest x-ray using posteroanterior view was performed, which revealed increase of right hemidiaphragm and images compatible with intestinal loop in the lower third of this hemithorax. Right traumatic diaphragmatic hernia was diagnosed. This is an infrequent disease due to the shock-absorbing effect of the liver. He was medically treated and one hour later, the pain ceased. Hernia was reduced spontaneously, which was confirmed in the posterior chest x-ray. He was further operated on electively and the final result was favorable(AU)

Hernia diafragmática traumática derecha / Right traumatic diaphragmatic hernia

Paciente masculino, de 47 años de edad que sufrió un accidente automovilístico en el año 1991, con fractura de columna lumbar , que dejó como secuela una paraparesia flácida postraumática con nivel neurológico de lesión del segmento L5, con disminución de la fuerza muscular y de la sensibilidad en las extremidades inferiores. Se le hizo inmovilización con yeso durante 6 meses y fue intervenido quirúrgicamente en ese propio año. Se le realizó fijación y osteosíntesis con material metálico. Se rehabilitó durante varios anos alcanzando buen fortalecimiento muscular y en noviembre de 2008, en horas de la noche, comienza con dolor intenso a nivel de hipocondrio y hemitórax derecho, que se incrementa con el decúbito supino y mejora con el decúbito lateral izquierdo y con disnea moderada. Al examen físico del tórax, se constató aumento de la matidez del tercio inferior del hemitórax derecho y se auscultaron ruidos hidroaéreos a este nivel. Se realizó radiografía (Rx) de tórax vista posteroanterior(PA), donde se constató elevación del hemidiafragma derecho e imagen compatible con presencia de asas intestinales en el tercio inferior de este hemitórax. Se diagnosticó una hernia diafragmática traumática derecha , que es una enfermedad poco frecuente debido al efecto amortiguador del hígado. Se realizó tratamiento médico inicialmente y una hora después , cesa el dolor. Se redujo la hernia de manera espontánea, lo que se corroboró en el Rx de tórax ( vista PA) evolutivo. Posteriormente fue intervenido quirúrgicamente de forma electiva y el resultado fue favorable(AU)

A 47 years-old male patient, who was injured in a car accident in 1991 and suffered lumbar column fracture that left as a sequel a postraumatic flaccid paraparesia with neurological lesion of L5 segment, reduction of muscle strength and sensitivity in lower limbs. He had plaster for 6 months and was surgically treated in that year. He underwent fixation and osteosynthesis with metal material. During several years, he went to rehabilitation program and finally achieved good muscle strengthening. In November 2008, he began feeling intense pain at hypochondrium and right hemithorax at night and also moderate dyspnea. On the physical exam, it was confirmed that there was increase of lower third of right hemithorax and hydroaerial noises were heard. Chest x-ray using posteroanterior view was performed, which revealed increase of right hemidiaphragm and images compatible with intestinal loop in the lower third of this hemithorax. Right traumatic diaphragmatic hernia was diagnosed. This is an infrequent disease due to the shock-absorbing effect of the liver. He was medically treated and one hour later, the pain ceased. Hernia was reduced spontaneously, which was confirmed in the posterior chest x-ray. He was further operated on electively and the final result was favorable(AU)

Congenital intrahepatic portosystemic venous shunt presenting with paraparesis as the initial symptom.

An 85-year-old woman was hospitalized with rapidly progressive paraparesis without altered consciousness, although she was not definitively diagnosed. She developed acute drowsiness and disorientation several days later. An intrahepatic portosystemic venous shunt (IPSVS) was observed on enhanced computed tomography, and hyperammonemia suggested leakage of neurotoxins from the shunt as the etiology of the patient's symptoms. Her neurological symptoms and hyperammonemia improved following transcatheter shunt embolization. We diagnosed her with hepatic myelopathy, which is a rare complication of liver cirrhosis and portosystemic venous shunts. Hepatic myelopathy resulting from a congenital IPSVS has not been previously reported. A diagnosis of hepatic myelopathy should be ruled out in diagnostically difficult cases of paraparesis.

Treatment of delayed neurological deficits after surgical repair of thoracic aortic aneurysm.

Delayed neurologic deficits, paraplegia and paraparesis, are devastating complications after repair of a descending thoracic and thoracoabdominal aortic aneurysm (TAAA). A treatment protocol has not been established, although strategies such as cerebrospinal fluid (CSF) drainage, maintaining blood pressure and medication have been described. Cerebrospinal drain status /oxygen delivery/patient status (COPS) therapy for delayed neurological deficit can improve spinal cord ischemia through reducing intraspinal pressure, improving oxygen delivery and maintaining high blood pressure. We describe one patient (Case 1), in whom descending thoracic and abdominal aortic aneurysms were treated by endovascular aortic repair, and another (Case 2) with Crawford type II TAAA, who developed delayed neurological deficits that were treated with immediate COPS therapy (Modified Tarlov scale; Case 1, improved from 2 to 4; Case 2, from 0 to 4). These findings indicate the benefit of COPS for treating delayed neurological deficits after descending thoracic and TAAA.

[Multiple sclerosis associated with antiphospholipid syndrome: diagnostic and therapeutic difficulties]. / Sclérose en plaques associée à un syndrome des antiphospholipides : difficultés diagnostiques et thérapeutiques.

Strokes are the main neurological manifestation of antiphospholipid syndrome. Other clinical presentations are possible and may mimic classic symptoms of multiple sclerosis (MS). A 46-year-old woman, with a history of two miscarriages, presented four subacute neurological episodes (optic neuritis, right facial paralysis, paraparesis of the thigh, and right brachial monoparesis). Using McDonald criteria, the diagnosis of multiple sclerosis was retained. Because of the occurrence of thrombocytopenia during a final relapse, we reconsidered the diagnosis of MS. Search for antiphospholipid antibodies was positive. All clinical manifestations and complementary tests were compatible with the diagnosis of antiphospholipid syndrome associated with multiple sclerosis. Given the great similarity of clinical, radiological and biological findings in the two diseases, non-thrombotic neurological manifestations of antiphospholipid syndrome can be difficult to distinguish from MS associated with antiphospholipid syndrome.

Painless transient paraparesis as the solitary manifestation of aortic dissection.

We present a 62-year-old man with acute and temporary paraparesis of the lower extremities as the solitary symptom of an anterior spinal artery syndrome caused by a type B aortic dissection. Ischemia of the spinal cord was confirmed by magnetic resonance imaging. Neurologic symptoms resolved completely within 6 hours and conservative treatment was successful up to 8 months follow-up. Our report illustrates that painless, transient neurologic deficit can be the only presenting symptom of acute aortic dissection and that aortic dissection should be part of the differential diagnosis of acute paraparesis.

Reversal of delayed-onset paraparesis after revision thoracic endovascular aortic repair for ruptured thoracic aortic aneurysm.

Thoracic endovascular aortic repair (TEVAR) is an important surgical option for the emergency treatment of ruptured thoracic aortic aneurysms, but is associated with a risk of spinal cord ischemia (SCI). Although risk factors for the development of SCI have been well described, the effectiveness of treatment to increase spinal cord perfusion pressure remains incompletely understood. We report the successful treatment of delayed-onset paraparesis after revision TEVAR for acute descending thoracic aortic rupture with the combined use of blood pressure augmentation and cerebrospinal fluid drainage. The clinical manifestations, pathophysiology, and management of SCI after TEVAR are reviewed.

A new syndrome sheds light on old medical & rehabilitative dilemmas: paraparesis due to rhabdomyolysis and bilaterally symmetric compartment syndrome in four patients. Cases study.

Via our description of a seemingly heterogeneous group of four patients who presented to our rehabilitation facility with a rather unusual clinical presentation of compartment syndrome with development of a flaccid paraparesis and rhabdomyolysis immediately after awakening from a prolonged sleep episode in an unusual posture - which might, in fact, be a 'new syndrome' - we have also come to address an important issue linking our group of patients - specifically, the complexities which present to a rehabilitative facility in the cases of unusual and unclear diagnoses. Eventually, all four of our patients remained severely disabled. All had suffered sensorimotor axonal demyelinative polyneuropathies and two patients had subclinical hypothyroidism. Prior to the prolonged sleep episode, they had all consumed alcohol and drugs. Using these four rather demanding diagnostic rehabilitative cases we address the ever-important issue of timely mutual communication and patience. For when a rehabilitative facility is confronted with patients whose diagnoses are not clear, the scope of the long-term comprehensive rehabilitation management faces some major obstacles with respect to how the rehabilitative team can succeed in designing a 'tailor-made' rehabilitation program for these patients, which often-times proves to be a rather tricky task requiring innovative and creative efforts on the parts of all those involved in the care of the patient. Quite a challenging task, indeed, yet one genuinely necessary to attempt to achieve so that the patient, family and, of course, the 'payer agency/provider' can all prepare themselves, realistically so as to obtain the best overall rehabilitative outcome for these patients. We conclude that what is most necessary for these unique patients is patience.

Resolution of neurological DCI after long treatment delays.

We report two interesting cases in which both divers sustained a very serious Type II decompression sickness. This involved substantial neurological impairment which was successfully treated despite having a delayed treatment time 12 hours or more. The treatment used hyperbaric oxygen recompression therapy with the addition oflidocaine i.v. drip. This first case was in November 2007 and the second was in December 2007 and both patients made excellent recoveries.

Spinal dural arteriovenous fistula in a case with lipomyelodysplasia.

Coexistence of a spinal dural arteriovenous fistula within a dysraphic spinal lesion is a very rare situation. We report a 40-year-old man who presented with low back pain and progressive paraparesis. MR images showed an intradural high signal intensity mass at the L2-L3 level containing irregular signal void structures. Spinal angiography revealed extradural arteriovenous fistula with three connections, drained by a tortuous perimedullary vein.