Syringomyelia and Arachnoiditis
Total Page:16
File Type:pdf, Size:1020Kb
Load more
Recommended publications
-
Tuberculous Optochiasmatic Arachnoiditis and Optochiasmatic Tuberculoma in Malaysia
Neurology Asia 2018; 23(4) : 319 – 326 Tuberculous optochiasmatic arachnoiditis and optochiasmatic tuberculoma in Malaysia ¹Mei-Ling Sharon TAI, 3Shanthi VISWANATHAN, 2Kartini RAHMAT, 4Heng Thay CHONG, ¹Wan Zhen GOH, ¹Esther Kar Mun YEOW, ¹Tsun Haw TOH, ¹Chong Tin TAN 1Division of Neurology, Department of Medicine; 2Department of Biomedical Imaging, Faculty of Medicine, University Malaya, Kuala Lumpur; 3Department of Neurology, Hospital Kuala Lumpur, Kuala Lumpur, Malaysia; 4Department of Neurology, Western Health, Victoria, Australia. Abstract Background & Objectives: Arachnoiditis which involves the optic chiasm and optic nervecan rarely occurs in the patients with tuberculous meningitis (TBM). The primary objective of this study was to determine the incidence, assess the clinical and neuroimaging findings, and associations, understand its pathogenesis of these patients, and determine its prognosis. Methods: The patients admitted with TBM in the neurology wards of two tertiary care hospitals from 2009 to 2017 in Kuala Lumpur, Malaysia were screened. The patients with OCA and optochiasmatic tuberculoma were included in this study. We assessed the clinical, cerebrospinal fluid (CSF), imaging findings of the study subjects and compared with other patients without OCA or optochiasmatic tuberculoma. Results: Eighty-eight patients with TBM were seen during the study period. Seven (8.0%) had OCA and one (1.1%) had optochiasmatic tuberculoma. Five out of seven (71.4%) patients with OCA were newly diagnosed cases of TBM. The other two (28.6%) had involvement while on treatment with antituberculous treatment (paradoxical manifestation). The mean age of the patients with OCA was 27.3 ± 11.7. All the OCA patients had leptomeningeal enhancement at other sites. All had hydrocephalus and cerebral infarcts on brain neuroimaging. -
Intractable Vomiting and Hiccups As the Presenting Symptom of Neuromyelitis Optica
Case Report Intractable vomiting and hiccups as the presenting symptom of neuromyelitis optica Girish Baburao Kulkarni, Pradeep Kallollimath, R. Subasree, M. Veerendrakumar Department of Neurology, National Institute of Mental Health and Neurosciences, Bangalore, Karnataka, India Abstract Vomiting and hiccups can be due to peripheral or central causes. Neurological diseases causing vomiting and hiccups are due to lesions of medulla involving area postrema and nucleus tractus solitarius. Neuromyelitis optica (NMO) is one such disease which involves these structures. However refractory vomiting and hiccups as the presenting symptom of NMO is unusual. Here we report a patient with NMO in whom refractory vomiting and hiccups were the sole manifestation of the first attack. Diagnosis can be missed at this stage leading to delay in treatment and further complications. This case demonstrates the importance of considering NMO in any patient presenting with refractory vomiting and hiccups and with local and metabolic causes ruled out and linear medullary lesion on magnetic resonance imaging may indicate the diagnosis even when the classical clinical criteria are not met. Anti NMO antibody testing should be done and if positive appropriate treatment should be initiated to prevent further neurological damage. Key Words Aquaporin antibody, hiccups, intractable vomiting, neuromyelitis optica For correspondence: Dr. Girish Baburao Kulkarni, Department of Neurology, National Institute of Mental Health and Neurosciences, Bangalore ‑ 560 029, Karnataka, -
Central Pain in the Face and Head
P1: KWW/KKL P2: KWW/HCN QC: KWW/FLX T1: KWW GRBT050-128 Olesen- 2057G GRBT050-Olesen-v6.cls August 17, 2005 2:10 ••Chapter 128 ◗ Central Pain in the Face and Head J¨orgen Boivie and Kenneth L. Casey CENTRAL PAIN IN THE FACE AND HEAD Anesthesia dolorosa denotes pain in a region with de- creased sensibility after lesions in the CNS or peripheral International Headache Society (IHS) code and diag- nervous system (PNS). The term deafferentation pain is nosis: used for similar conditions, but it is more commonly used in patients with lesions of spinal nerves. 13.18.1 Central causes of facial pain 13.18.1 Anesthesia dolorosa (+ code to specify cause) 13.18.2 Central poststroke pain EPIDEMIOLOGY 13.18.3 Facial pain attributed to multiple sclerosis 13.18.4 Persistent idiopathic facial pain The prevalence of central pain varies depending on the un- 13.18.5 Burning mouth syndrome derlying disorder (Tables 128-1 and 128-2) (7,29). In the ab- 13.19 Other centrally mediated facial pain (+ code to sence of large scale epidemiologic studies, only estimates specify etiology) of central pain prevalence can be quoted. In the only prospective epidemiologic study of central Note that diagnosis with IHS codes 13.18.1, 13.18.4, and pain, 191 patients with central poststroke pain (CPSP) 13.18.5 may have peripheral causes. were followed for 12 months after stroke onset (1). Sixteen World Health Organization (WHO) code and diagnosis: (8.4%) developed central pain, an unexpectedly high inci- G 44.810 or G44.847. -
Le Journal Canadien Des Sciences Neurologiques
LE JOURNAL CANADIEN DES SCIENCES NEUROLOGIQUES tations of ambulatory cassette recordings, computer application edge may lead to the rapid productive careers of young clinical for data reduction and seizure and spike recognition, and the investigators and scientists being replaced sooner by the next power and pitfalls of monitoring techniques in differentiating group of young Turks. "fits from faints". Broad applications including the pre-surgical The clinical reviews of cases by Jonesco-Sisesti are painstaking, evaluation are well-covered. Although some chapters give good and it's salutary to again see the careful clinical observation descriptions of subcategories of primary generalized and com that formed the basis of modern neurology. How long has it plex partial seizures, this material is available in other more been since we saw someone recording Oppenheim's, Gordon's, general texts on epilepsy. Schaeffer's reflexes as part of the clinical examination. One Unfortunately, I feel the weaknesses outweigh the qualities must pause when reading that the "mediopublic reflex pro of the book. There should be a more clear definition of research duced a definite inferior response and a weak superior response", versus routine clinical application of the technology. Through but the pause is enjoyable as it recalls the impeccable respect out the book the value of such monitoring is repeatedly stressed, for the neurological examination prior to the age of technology. yet there are no controlled studies to support its superiority Dr. Ross was given the idea for this project may years ago by over conventional clinical and EEG evaluations. The case for the late Dr. -
Thoracic Syringomyelia in a Patient with Amyotrophic Lateral Sclerosis
International Neuropsychiatric Disease Journal 3(4): 136-140, 2015; Article no.INDJ.2015.019 ISSN: 2321-7235 SCIENCEDOMAIN international www.sciencedomain.org Thoracic Syringomyelia in a Patient with Amyotrophic Lateral Sclerosis Daniele Lo Coco1,2, Rossella Spataro2, Alfonsa Claudia Taiello2 and Vincenzo La Bella2* 1Neurology Unit, Civico General Hospital ARNAS, 90127, Palermo, Italy. 2Department of Experimental Biomedicine and Clinical Neurosciences, ALS Clinical Research Center, University of Palermo, Via G. La Loggia 1, 90129 Palermo, Italy. Authors’ contributions This work was carried out in collaboration between both authors. Authors DLC and VLB made the diagnosis and outlined the case report. Authors DLC, RS, and ACT managed the literature search and wrote the first draft of the manuscript with assistance from author VLB. All authors read and approved the final manuscript. Article Information DOI: 10.9734/INDJ/2015/17176 Editor(s): (1) Zhefeng Guo, Department of Neurology, University of California, Los Angeles, USA. Reviewers: (1) Mario Ciampolini, Università di Firenze, Department of Peiatrics, Università di Firenze, Italy. (2) Raghvendra Vijay Ramdasi, Jaslok Hospital & Research Centre, Mumbai India. Complete Peer review History: http://www.sciencedomain.org/review-history.php?iid=840&id=29&aid=8665 Received 1st March 2015 th Short Communication Accepted 20 March 2015 Published 2nd April 2015 ABSTRACT We report a patient with bulbar-onset, clinically defined, sporadic amyotrophic lateral sclerosis bearing an isolated syringomyelia of the lower thoracic portion of the spinal cord. This is a very unusual association between two rare and progressive disorders, both affecting the spinal motoneurons. Syringomyelia might have acted as a phenotypic modifier in this ALS patient. -
Outcomes in Children Undergoing Posterior Fossa Decompression And
CLINICAL ARTICLE J Neurosurg Pediatr 25:21–29, 2020 Outcomes in children undergoing posterior fossa decompression and duraplasty with and without tonsillar reduction for Chiari malformation type I and syringomyelia: a pilot prospective multicenter cohort study *Joyce Koueik, MD, MS,1 Carolina Sandoval-Garcia, MD,1 John R. W. Kestle, MD,2 Brandon G. Rocque, MD, MS,3 David M. Frim, MD, PhD,4 Gerald A. Grant, MD,5 Robert F. Keating, MD,6 Carrie R. Muh, MD,7 W. Jerry Oakes, MD,3 Ian F. Pollack, MD,8 Nathan R. Selden, MD, PhD,9 R. Shane Tubbs, PhD, PA-C,3 Gerald F. Tuite, MD,10 Benjamin Warf, MD,11 Victoria Rajamanickam, MS,12 Aimee Teo Broman, MA,12 Victor Haughton, MD,13 Susan Rebsamen, MD,13 Timothy M. George, MD,14 and Bermans J. Iskandar, MD1 1Department of Neurological Surgery, University of Wisconsin, Madison, Wisconsin; 2Department of Neurosurgery, University of Utah, Salt Lake City, Utah; 3Department of Neurosurgery, Children’s of Alabama, Birmingham, Alabama; 4Section of Neurosurgery, Department of Surgery, University of Chicago, Chicago, Illinois; 5Department of Pediatric Neurosurgery, Stanford Health Care, Palo Alto, California; 6Department of Neurosurgery, Children’s National Health System, Washington, DC; 7Department of Neurosurgery, Duke University Medical Center, Durham, North Carolina; 8Department of Neurosurgery, UPMC Children’s Hospital of Pittsburgh, Pennsylvania; 9Department of Neurological Surgery, Oregon Health and Science University, Portland, Oregon; 10Department of Neurosurgery, Johns Hopkins All Children’s Hospital, Tampa, Florida; 11Department of Neurosurgery, Boston Children’s Hospital, Boston, Massachusetts; Departments of 12Biostatistics and Medical Informatics and 13Radiology, University of Wisconsin–Madison, Wisconsin; and 14Department of Neurosurgery, Dell Medical School, Austin, Texas OBJECTIVE Despite significant advances in diagnostic and surgical techniques, the surgical management of Chiari malformation type I (CM-I) with associated syringomyelia remains controversial, and the type of surgery performed is surgeon dependent. -
Spinal Arachnoiditis Stephen I
THE CANADIAN JOURNAL OF NEUROLOGICAL SCIENCbS REVIEW ARTICLE: Spinal Arachnoiditis Stephen I. Esses and T.P. Morley SUMMARY: A review of the literature points to the many causes of arachnoiditis and the failure of treatment to arrest or reverse its effects. The true incidence cannot be determined, although it is probably lower than might at first appear from the published articles. In the radiological literature the diagnosis seems to derive from an examination of the films alone, often without reference to the clinical findings or appearance at operation. While attempts at treatment are usually unsuccessful, some iatrogenic cases can be prevented by the avoidance of intrathecal steroid injections or unduly rough or repeated surgical exploration of the lumbar vertebral canal. RESUME: Une revue de la litterature indique clairement que I'arachnoidite peut etre due a plusieurs causes et que son traitement est deficitaire. L'incidence reelle de I'arachnoidite ne peut etre determinee, mais elle est probablement inferieure au taux apparent selon les publications. Ainsi dans la litterature radiologique on semble etablir un diagnostic sur la base des films sans tenir compte des aspects clini- ques ou de la presentation chirurgicale. Quoique les essais therapeutiques soient generalement negatifs, on peut prevenir certaines causes iatrogeniques en evitant les injections intrathecals de steroides ou les explorations repetees, ou trop dures, du canal vertebral lombaire. Can. J. Neurol. Sci. 1983; 10:2-10 Feodor Krause (1907) was the first to describe adhesive dense collagen deposition which completely encases the lumbar arachnoiditis. By 1936 Elkington presented a com nerve roots. The roots are deprived of their blood supply plete analysis of forty-one cases under the tide "Meningitis and undergo progressive atrophy. -
Syringomyelia in Cervical Spondylosis: a Rare Sequel H
THIEME Editorial 1 Editorial Syringomyelia in Cervical Spondylosis: A Rare Sequel H. S. Bhatoe1 1 Department of Neurosciences, Max Super Specialty Hospital, Patparganj, New Delhi, India Indian J Neurosurg 2016;5:1–2. Neurological involvement in cervical spondylosis usually the buckled hypertrophic ligament flavum compresses the implies radiculopathy or myelopathy. Cervical spondylotic cord. Ischemia due to compromise of microcirculation and myelopathy is the commonest cause of myelopathy in the venous congestion, leading to focal demyelination.3 geriatric age group,1 and often an accompaniment in adult Syringomyelia is an extremely rare sequel of chronic cervical patients manifesting central cord syndrome and spinal cord cord compression due to spondylotic process, and manifests as injury without radiographic abnormality. Myelopathy is the accelerated myelopathy (►Fig. 1). Pathogenesis of result of three factors that often overlap: mechanical factors, syringomyelia is uncertain. Al-Mefty et al4 postulated dynamic-repeated microtrauma, and ischemia of spinal cord occurrence of myelomalacia due to chronic compression of microcirculation.2 Age-related mechanical changes include the cord, followed by phagocytosis, leading to a formation of hypertrophy of the ligamentum flavum, formation of the cavity that extends further. However, Kimura et al5 osteophytic bars, degenerative disc prolapse, all of them disagreed with this hypothesis, and postulated that following contributing to a narrowing of the spinal canal. Degenerative compression of the cord, there is slosh effect cranially and kyphosis and subluxation often aggravates the existing caudally, leading to an extension of the syrinx. It is thus likely compressiononthespinalcord.Flexion–extension that focal cord cavitation due to compression and ischemia movements of the spinal cord places additional, dynamic occurs due to periventricular fluid egress into the cord, the stretch on the cord that is compressed. -
A Histopathological and Immunohistochemical Study of Acute and Chronic Human Compressive Myelopathy
Cellular Pathology and Apoptosis in Experimental and Human Acute and Chronic Compressive Myelopathy ROWENA ELIZABETH ANNE NEWCOMBE M.B.B.S. B.Med Sci. (Hons.) Discipline of Pathology, School of Medical Sciences University of Adelaide June 2010 A thesis submitted in partial fulfilment of the requirements for the degree of Doctor of Philosophy CHAPTER 1 INTRODUCTION 1 The term “compressive myelopathy” describes a spectrum of spinal cord injury secondary to compressive forces of varying magnitude and duration. The compressive forces may act over a short period of time, continuously, intermittently or in varied combination and depending on their magnitude may produce a spectrum varying from mild to severe injury. In humans, spinal cord compression may be due to various causes including sudden fracture/dislocation and subluxation of the vertebral column, chronic spondylosis, disc herniation and various neoplasms involving the vertebral column and spinal canal. Neoplasms may impinge on the spinal cord and arise from extramedullary or intramedullary sites. Intramedullary expansion producing a type of internal compression can be due to masses created by neoplasms or fluid such as the cystic cavitation seen in syringomyelia. Acute compression involves an immediate compression of the spinal cord from lesions such as direct trauma. Chronic compression may develop over weeks to months or years from conditions such as cervical spondylosis which may involve osteophytosis or hypertrophy of the adjacent ligamentum flavum. Compressive myelopathies include the pathological changes from direct mechanical compression at one or multiple levels and changes in the cord extending multiple segments above and below the site of compression. Evidence over the past decade suggests that apoptotic cell death in neurons and glia, in particular of oligodendrocytes, may play an important role in the pathophysiology and functional outcome of human chronic compressive myelopathy. -
ICD9 & ICD10 Neuromuscular Codes
ICD-9-CM and ICD-10-CM NEUROMUSCULAR DIAGNOSIS CODES ICD-9-CM ICD-10-CM Focal Neuropathy Mononeuropathy G56.00 Carpal tunnel syndrome, unspecified Carpal tunnel syndrome 354.00 G56.00 upper limb Other lesions of median nerve, Other median nerve lesion 354.10 G56.10 unspecified upper limb Lesion of ulnar nerve, unspecified Lesion of ulnar nerve 354.20 G56.20 upper limb Lesion of radial nerve, unspecified Lesion of radial nerve 354.30 G56.30 upper limb Lesion of sciatic nerve, unspecified Sciatic nerve lesion (Piriformis syndrome) 355.00 G57.00 lower limb Meralgia paresthetica, unspecified Meralgia paresthetica 355.10 G57.10 lower limb Lesion of lateral popiteal nerve, Peroneal nerve (lesion of lateral popiteal nerve) 355.30 G57.30 unspecified lower limb Tarsal tunnel syndrome, unspecified Tarsal tunnel syndrome 355.50 G57.50 lower limb Plexus Brachial plexus lesion 353.00 Brachial plexus disorders G54.0 Brachial neuralgia (or radiculitis NOS) 723.40 Radiculopathy, cervical region M54.12 Radiculopathy, cervicothoracic region M54.13 Thoracic outlet syndrome (Thoracic root Thoracic root disorders, not elsewhere 353.00 G54.3 lesions, not elsewhere classified) classified Lumbosacral plexus lesion 353.10 Lumbosacral plexus disorders G54.1 Neuralgic amyotrophy 353.50 Neuralgic amyotrophy G54.5 Root Cervical radiculopathy (Intervertebral disc Cervical disc disorder with myelopathy, 722.71 M50.00 disorder with myelopathy, cervical region) unspecified cervical region Lumbosacral root lesions (Degeneration of Other intervertebral disc degeneration, -
Benign Lumbar Arachnoiditis: MR Imaging with Gadopentetate Dimeglumine
763 Benign Lumbar Arachnoiditis: MR Imaging with Gadopentetate Dimeglumine Carl E. Johnson 1.2 MR imaging was performed in 13 patients with benign lumbar arachnoiditis both Gordon Sze3 before and after IV injection of gadopentetate dimeglumine. The arachnoiditis was proved by previous myelography in 12 patients and by noncontrast MR imaging in one patient. The disease was presumably the result of previous myelography and for surgery. It was characterized as mild in two patients, moderate in two patients, and severe in nine patients. Imaging was performed on a 1.5-T unit, and both short and long TR images were obtained before and after contrast administration. Noncontrast MR images demonstrated changes consistent with arachnoiditis in all patients. After contrast, three patients had no enhancement, three patients had minimal enhancement, three patients had mild enhancement, and four patients had moderate enhancement. In no case did contrast enhancement alter the diagnosis or reveal additional findings that could not be seen on the noncontrast images. Gadopentetate dimeglumine enhancement plays little role in the diagnosis of lumbar arachnoiditis. If used for another reason, however, short TR scans may show enhance ment of adherent roots in some cases. In addition, administration of gadopentetate dimeglumine will not cause sufficient enhancement to hinder the detection of arachnoid itis on long TR images and may aid in recognition of adherent roots on short TR images. AJNR 11:763-770, July/August 1990; AJR 155: October 1990 Previous work has shown the utility of gadopentetate dimeglumine in the MR imaging evaluation of neoplastic extradural, intradural, extramedullary, and intra medullary spinal disease [1-7]. -
JMSCR Vol||08||Issue||11||Page 472-476||November 2020
JMSCR Vol||08||Issue||11||Page 472-476||November 2020 http://jmscr.igmpublication.org/home/ ISSN (e)-2347-176x ISSN (p) 2455-0450 DOI: https://dx.doi.org/10.18535/jmscr/v8i11.81 Cryptococcal meningoencephalitis leading to Binocular visual loss and paraparesis in a patient with advanced HIV Authors Akhil Deshmukh1, Amod Rajendran2, Aravind Reghukumar3*, Athul Gurudas4, Kiran Kumar5 1,2,4,5Department of Internal medicine, Medical College, Thiruvananthapuram, Kerala, India 3Head of the Department of Infectious Diseases, Government Medical College, Thiruvananthapuram, Kerala, India *Corresponding Author Aravind Reghukumar Head of the Department of Infectious Diseases, Government Medical College, Thiruvananthapuram, Kerala, India Abstract Cryptococcus neoformans is the most common invasive fungal infection of the central nervous system in patients with advanced HIV. Neurocryptococcosis usually presents as diffuse meningoencephalitis with ocular involvement occurring as a secondary phenomenon is up to 30 % of cases. Binocular visual loss due to cryptococcal meningoencephalitis being very rare, this case report describes a patient with advanced HIV who developed binocular visual loss and paraparesis as a complication of cryptococcaemia. Even though mechanisms of visual complications in cryptococcal meningitis are still unclear, intracranial hypertension is postulated to be the primary cause while leads to delayed onset of visual loss. Our patient had early onset of binocular painless visual loss in the absence of papilloedema Patient also had features of cryptococcal spinal arachnoiditis which manifested as asymmetric lower limb weakness with urinary retention. In view of binocular visual loss and spinal arachnoiditis, adjunctive corticosteroids were added to the treatment regime consisting of amphotericin deoxycholate and flucytosine, following which the patient made a gradual clinical recovery.