Babinski's hand sign: many have tried / O sinal de Babinski na mão: muitos têm tentado

ABSTRACT Recognizing the semiologic importance of the second, and most famous, sign described by Joseph Babinski - the extension of the hallux after stimulation of the plantar region in order to differentiate organic from pithiatic paralysis- several authors have tried to find a comparable signal in the hand. After 122 years, no one has succeeded.

RESUMO Reconhecida a importância semiológica do segundo e mais famoso sinal descrito por Joseph Babinski - a extensão do hálux após estimulo plantar visando diferenciar a paralisia orgânica da pitiática - diversos autores vêm tentando encontrar um sinal equiparável na mão. Após 122 anos ninguém conseguiu obter sucesso.

Neuroparacoccidioidomycosis: Case Report and Literature Review

Introduction Paracoccidioidomycosis (PCM) is a systemic mycosis caused by the fungus Paracoccidioides brasiliensis, and it can compromise the central nervous system (CNS) in 10­27% of all cases. Case Report A 31-year-old man presented to the Emergency Department with headache, left-sided weakness, clonus at the ankle and a positive Babinski sign. Head computed tomography (CT) and magnetic resonance imaging (MRI) scans showed a 5.1 3.8 cm lobulated lesion with areas of liquefaction in the right centrum semiovale. Discussion Central nervous system PCM can mimic a brain tumor, and most cases are diagnosed by biopsy of the lesion. The treatment includes antibiotics, but some cases require surgery. Conclusion Due to high morbimortality rates, the diagnosis must be considered, and early treatment started in patients who live in rural regions endemic for PCM when a ring-enhancing mass associated with perilesional edema is observed on MRI scans.

Introdução Paracoccidioidomicose (PCM) é uma micose sistêmica causada pelo fungo Paracoccidioides brasiliensis e que pode comprometer o sistema nervoso central (SNC) em 10­27% dos casos. Relato de caso Um homem de 31 anos é admitido no pronto socorro com cefaleia, hemiparesia esquerda com clonus e presença de sinal de Babinski. As imagens da tomografia computadorizada (TC) de crânio e da ressonância nuclear magnética (RNM) demonstraram uma lesão de 5,1 3,8 cm no centro semioval direito de aspecto lobulado com áreas de liquefação no centro semioval direito. Discussão Paracoccidioidomicose do SNC pode simular um tumor cerebral, sendo a maioria dos casos diagnosticada por biopsia da lesão. O tratamento inclui antibióticos, mas alguns casos necessitam de abordagem cirúrgica. Conclusão Devido à alta morbimortalidade, o diagnóstico deve ser considerado e o tratamento precoce iniciado em pacientes que vivem em áreas rurais endêmicas para PCM e que apresentam lesão com captação anelar de contraste associada a edema perilesional nas imagens de RNM.

A Case of Acute Hemorrhagic Encephalomyelitis associated with Mycoplasma Pneumoniae Infection / 대한소아신경학회지

Acute hemorrhagic encephalomyelitis (AHEM) is a severe form of encephalitis characterized by fulminant clinical course and presence of hemorrhagic necrosis of the white matter. Mycoplasma pneumoniae (M. pneumoniae) have severe central nervous syndrome complication with encephalitis as that most common pediatric manifestations, but have been extremely rare report with AHME. A 10-year-old boy was referred to emergency room because of drowsy mental status, weakness of left side extremities and truncal ataxia. His deep tendon reflexes were hyperactive, neck stiffness sign and Babinski sign were both positive. Motor power were decreased on the both left upper and lower extremities. The sequences of T2-weighted and gradient recalled echo (GRE) showed hyper-intense lesions on multifocal white natter areas with hemorrhagic signal. Cerebrospinal fluid (CSF) analysis showed the pleocytosis with neutrophil dominant. The results of deoxyribonucleic acid (DNA) test and culture of M. pneumoniae were reported negative in CSF, but immunoglobulin M (IgM) was positive in blood. He received intravenous high dose corticosteroid and macrolide. After discharge, his neurologic function gradually returned to normal including sitting and standing without support. We reported the previously healthy boy with M. pneumonia related AHEM. The early diagnosis with brain MRI and the aggressive immunosuppressive treatment may be beneficial for recovery.

A Long, Solitary, Rosary-Shaped Spinal Neurofibroma

STUDY DESIGN: Case report. OBJECTIVES: We report the case of a long, solitary, rosary-shaped neurofibroma that was misdiagnosed as another disease due to the patient's surgical history involving repetitive procedures and its abnormal appearance. SUMMARY OF LITERATURE REVIEW: Neurofibroma is an intradural-extramedullary spinal tumor. It is generally not difficult to diagnose due to its frequent occurrence and specific magnetic resonance imaging (MRI) findings. However, to date, neurofibromatosis stigmata and long, solitary, rosary-shaped neurofibromas have rarely been reported. MATERIALS AND METHODS: A 60-year-old woman was admitted to our hospital due to persistent pain, despite previous surgery and repetitive procedures. On physical examination, vision loss, hearing loss, skin discoloration, or subcutaneous nodules were not observed. A neurologic examination revealed normal motor and sensory function and voiding sensation. No pathologic reflexes such as the Babinski sign were observed. Previous sequential MRIs revealed intradural lesions that progressed from the thoracic vertebra 11 to the lumbar vertebra 3. She had no signs of neurofibromatosis stigmata, and the neurologic examination was unremarkable. The initial diagnosis was based on serial MRIs, which revealed a parasite infestation, a spinal cord tumor (myxopapillary-type ependymoma with hemorrhage), arachnoiditis, and vascular malformations. Total mass excision was performed, and the final diagnosis was neurofibroma. RESULTS: There were no signs of a tumor remnants or local recurrence in a 1-year follow-up MRI study. CONCLUSIONS: Although intradural spinal tumors are very rare, their clinical features are nonspecific and resemble other degenerative spinal diseases, including spinal stenosis and disc herniation. These diseases may easily be overlooked by physicians.

Afectación cerebral en la granulomatosis de Wegener. Reporte de caso / Brain involvement in Wegener's granulomatosis. Case report

La granulomatosis con poliangeítis (GPA) ­antes denominada granulomatosis de Wegener­ es una enfermedad autoinmunitaria multisistémica poco frecuente, de etiología desconocida. En esta enfermedad el compromiso del sistema nervioso central es muy raro aunque tiene mucha importancia porque se relaciona con períodos refractarios. El diagnóstico diferencial de las manifestaciones cerebrales de la GPA es difícil porque no hay signos radiográficos excluyentes de otras lesiones intra o extra-axiales. Este artículo presenta el caso de un paciente con granulomatosis de Wegener de larga evolución, que debuta con crisis convulsivas y focalidad neurológica secundarias a una lesión intraaxial parietal izquierda. Las características sintomáticas, histopatológicas y radiográficas se describen cuidadosamente y se discute el papel de la cirugía para esclarecer el diagnóstico en este paciente. (AU)

The granulomatosis with polyangiitis (GPA), known before as Wegener's granulomatosis, is an autoimmune multisystemic disease, not so common, of unknown etiology. The compromise of this particular disease to the neurological central system is very rare although it's very important because of its relationship with refractory disease periods. The differential diagnosis of the manifestations of the GPA at cerebral level it's not easy to see because there are not that allows the exclusion of other lesions intra or extra axials. We present the case of the patient with Wegener granulomatosis of long evolution that begins with seizures and motor deficit secondary to a left parietal intra axial mass. The clinical characteristics histopathological and radiological are careful described and the role of surgery in management is discussed. (AU)

Cervical Myelopathy Caused by Intracranial Dural Arteriovenous Fistula

Intracranial dural arteriovenous fistula (dAVF) usually results in various problems in the brain. But it can be presented as a myelopathy, which may make early diagnosis and management to be difficult. We recently experienced a case of cervical myelopathy caused by intracranial dAVF. A 60-year-old man presented with a 3-year history of gait disturbance due to a progressive weakness of both legs. Neurological examination revealed spastic paraparesis (grade IV) and Babinski sign on both sides. Magnetic resonance imaging showed serpentine vascular signal voids at C2-T1 on T2-weighted image with increased signal intensity and swelling of spinal cord at C1-C4. We performed a brain computed tomography angiography and found intracranial dAVF with multiple arteriovenous shunts. Venous drainages were noted at tentorial veins and cervical perimedullary veins. After Onyx embolization, the patient showed gradual improvement in motor power and gait disturbance. The venous drainage pattern is a well-known prognostic factor of dAVF. In our case, the intracranial dAVF drained to spinal perimedullary vein, which seemed to result in the ischemic myelopathy. Although it is rare condition, it sometimes can cause serious complications. Therefore, we should keep in mind the possibility of intracranial dAVF when a patient presents myelopathy.

Delayed Surgery for Aortic Dissection after Intravenous Thrombolysis in Acute Ischemic Stroke

We report a case of aortic dissection masquerading as acute ischemic stroke followed by intravenous thrombolysis. A 59-year-old man presented with dizziness. After examination, the patient had a seizure with bilateral Babinski signs. Soon after identifying multiple acute infarctions in both hemispheres on diffusion-weighted brain magnetic resonance (MR) imaging, tissue plasminogen activator (t-PA) was administered. Both common carotid arteries were invisible on MR angiography, and subsequent chest computed tomography revealed an aortic dissection. The emergency operation was delayed for 13 hours due to t-PA administration. The patient died of massive bleeding.

Hepatic Encephalopathy With Corticospinal Tract Involvement Demonstrated by Diffusion Tensor Tractography

A 50-year-old man with liver cirrhosis and esophageal varix for 3 years was diagnosed with hematemesis and treated for a bleeding varix. However, bleeding recurred 11 days later, and he developed drowsiness with left hemiparesis. His left upper and lower extremity muscle strengths based on the manual muscle test at the onset were grade 2/5 and 1/5, respectively. The Babinski sign was positive. His serum ammonia level was elevated to 129.9 microg/dL (normal, 20-80 microg/dL). Magnetic resonance imaging revealed restriction on diffusion and T2-hyperintensities with decreased apparent diffusion coefficient values in the bilateral frontoparietooccipital cortex. The effect was more severe in the right hemisphere and right parietooccipital cortices, which were compatible with hepatic encephalopathy. Although the patient's mental status recovered, significant left-sided weakness and sensory deficit persisted even after 6 months. Diffusion tensor tractography (DTT) performed 3 months post-onset showed decreased volume of the right corticospinal tract. We reported a patient with hepatic encephalopathy involving the corticospinal tract by DTT.

Doze sinais de Babinski: História da Neurologia e Neurossemiologia / Babinski’s twelve signs: History of Neurology and Neurosemiology

Este artigo tem como finalidade contar um pouco da história daquele que é considerado o pai de semiologia neurológica, e relembrar doze dosseus sinais, a maioria dos quais voltados para a diferenciação entre as doenças orgânicas e conversivas.

This article aims to tell a small story of who is considered the ?father of neurological examination?, and remember twelve of his signs, most of which focused on the differentiation between organic diseases and hysteria.

How many Babinski's signs are there? / Quantos sinais de Babinski existem?

In addition to the famous sign described by Joseph Babinski, which is also known as Babinski's reflex, there are references in the literature to various other signs described by this famous disciple of J-M Charcot. This article reviews all the neurological signs described by Babinski.

Além do famoso sinal descrito por Joseph Babinski, também definido como reflexo de Babinski, existem referências na literatura mundial de vários outros sinais descritos pelo famoso discípulo de J-M Charcot. Este artigo apresenta uma revisão de todos os sinais neurológicos descritos pelo professor Babinski.

Two Babinski signs in seropositive (HAM) and seronegative tropical spastic paraparesis / Dos signos de Babinski en pacientes con paraparesia espástica tropical seropositiva (HAM) y seronegativa

Tropical spastic paraparesis (TSP) may or may not be associated to HTLV-I antibodies and is usually characterized by clinical and pathological spinal cord abnormalities at thoracic levels. We present here five Brazilian patients who had typical chronic idiopatic spastic paraparesis; two of them were HTLV-I seropositive (HAM) and three HTLV-I seronegative (TSP) - associated-myelopathy. Three out of these five patients also displayed clinical supraspinal involvement, indeed, platysma muscle hypotrophy or atrophy (the Babinski plus sign). These findings support the view that clinical involvement in HAM and TSP is wider than the spinal cord abnormalities usually considered. Possible non-infectious co-factors (e.g., mycotoxins) may be involved in disease pathogenesis in a multistep process of viruses, toxins and environment which may account for serological differences found in this group of patients.

La paraparesia espástica tropical (PET), puede o no estar asociada con anticuerpos contra el HTLV-I y se caracteriza, usualmente, por alteraciones clínicas y patológicas a nivel de region dorso-lumbar de la medula espinal. Presentamos cinco pacientes brasileros, quienes tuvieron hallazgos típicos de paraparesia espástica crónica idiopática; dos de ellos tuvieron (HAM) y tres no tuvieron (TSP) anticuerpos, en el suero, contra el HTLV-I. En tres pacientes se encontró hipotrofia o atrofia del músculo platisma (signo de Babinski plus), demostrando que el compromiso clínico en pacientes con HAM y TSP se extiende más allá de la médula espinal torácica. Cofactores (por ejemplo, micotoxinas) podrían estar involucrados en la patogénesis de esta enfermedad, en una interacción compleja de virus, toxinas y medio ambiente, lo cual explicaría las diferencias serológicas encontradas en este grupo de pacientes.

Babinski's signe de l'eventail: a turning point in the history of neurology

PURPOSE: The Babinski sign is a finding known since the start of the teachings of physical diagnosis by almost all medical students. This reflex is an incredibly helpful phenomenon that enables physicians to distinguish between central and the peripheral nervous system diseases right at the bedside. Yet, most students as well as physicians remain oblivious to the remarkable history behind the Babinski sign and what it means to evolutional history of the modern neurological exam. We intend to study the birth of the "signe de l'eventail" (the fanning sign) and how it transformed medical diagnosis as we practice it today. METHODS: An extensive search was conducted through the Internet to identify historical documents referring to Babinski and other physicians who also observed the phenomenon as early as the 17th and 18th century. We also conducted a search through medical journals that examined the Babinski sign and its history. RESULTS: The Babinski reflex had been observed much earlier than 1896, when Babinski referred to his finding for the first time. The reflex had been reported in the literature as far back as 1784 and afterwards reobserved several times before Babinski. However, it was Babinski who first offered an interpretation of the reflex and suggested that it was related to an organic disruption in the central nervous system. By identifying the sign, Babinski separated himself from Charcot in the sense of creating a new tradition in neurology where the findings in a neurological exam were of far more importance than just a plain history as his mentor had relied upon. CONCLUSIONS: Babinski was not only responsible for suggesting the significance of such sign, but also transformed the role that physical diagnosis plays in modern medicine, where physical examination is key in revealing underlying pathology.

Hemiplejía con dos signos de Babinski / Hemiplegia with two Babinski´s sign

La evaluación semiológica apropiada es uno de los aspectos más importantes para realizar un adecuado diagnóstico neurológico. Presentamos una paciente colombiana de 60 años de edad, quien padeció un infarto de la arteria cerebral media izquierda, originándole hemiplejía derecha, afasia motora, parálisis facial "central" derecha y atrofia del músculo platisma derecho. Este último hallazgo, originalmente descrito por Joseph Babinski, el cual es el verdadero signo de Babinski, no fue identificado sino hasta dos años y siete meses después de haberse presentado el ictus, aunque había sido evaluada, previamente, por diferentes especialistas en ciencias neurológicas. La no identificación de signos como el mencionado aquí lleva, en ocasiones, a realizar diagnósticos erróneos o incompletos afectando no sólo la localización apropiada de las lesiones sino, también, las eventuales medidas que se deben tomar en la neurorrehabilitación de estos pacientes.

Neurological signs and symptoms are very important to establish a correct neurological diagnosis. We present here a Colombian female patient, 60 yearsold, who had ischaemic stroke in the left cerebral media artery. It produced right hemiplegia, motor aphasia, "central" facial palsy and atrophy of right platysma muscle. This latter finding, described originally by Joseph Babinski as "The Babinski Sign" was observed only two years and seven months after the ictus even when she had, previously, been evaluated by several neurologists. The underdiagnosis of clinical signs like the one described here may lead to erroneous diagnosis that will, ultimately, affect neurorehabilitation measures.

Sinais de Babinski e Chaddock sem disfunção piramidal aparente / Babinski and Chaddock signs without apparent pyramidal disfunction

OBJETIVO: Verificar a presença dos sinais de Babinski e de Chaddock em cem pacientes sem história ou indícios clínicos de comprometimento da via piramidal, internados no Serviço de Clínica Médica do Hospital Universitário Clementino Fraga Filho da Universidade Federal do Rio de Janeiro. Como objetivos secundários, observar a possível prevalência de um sinal sobre o outro, assim como a influência da posição da cabeça sobre as respostas obtidas. MÉTODO: Cada um dos sinais foi pesquisado por um único autor, utilizando o mesmo instrumento, estando os pacientes em decúbito dorsal e com a cabeça em três posições. RESULTADOS: Em dez pacientes (10 por cento) obteve-se a resposta de extensão do hálux uni ou bilateral. O sinal de Babinski apresentou-se 18 vezes (40 por cento) e o sinal de Chaddock 27 vezes (60 por cento). CONCLUSÃO: O sinal de Chaddock foi o mais freqüente. As respostas anormais ocorreram duas vezes mais à esquerda e, aparentemente, não houve interferência da posição cefálica em relação às respostas obtidas.

A Case of HELLP Syndrome with Liver Infarction and Cerebral Venous Thrombosis

We describe a rare case of cerebral venous thrombosis and liver infarction with HELLP syndrome in a 25-year-old woman with eclampsia. She had complained of epigastric pain and had visited a local hospital for treatment. Also, signs of fetal distress were presented. After an emergency cesarean section, generalized tonic-clonic seizure occurred twice at a 10-minute interval. The patients was transferred to our emergency room, and the neurologic examination at that time, revealed a deep drowsy mentality and positive Babinski's sign; the deep tendon reflex was two positive. The laboratory findings revealed thrombocytopenia, an elevated liver function test, abnormal coagulation profiles. A bilateral ischemic change with left basal ganglia hemorrhage was seen on brain CT, and multiple foci of ill defined low-density lesions, mainly in the subcapsular portion of the liver and perivascular space, were visible on the abdominal CT. There was a faint showing of the deep venous system on the angiogram of both carotid arteries and a cerebral venous thrombosis was confirmed by using 4-vessel angiography. During the following 2 days, the cerebral hemorrhage and the low-density lesion were resolved through applications of heparin, and the patient returned to a nearly alert mental status. Finally she died of a hemorrhagic shock as a complication of disseminated intravascular coagulation.

A Case of Guillain-Barre Syndrome Presented with Isolated Internal Ophthalmoplegia and Babinski Sign

No abstract available.

The Clinical Properties of Deep Small Basal Ganglia Infarctions: Lacune or Small Striatocapsular Infarction?

BACKGROUND: Small subcortical infarctions of basal ganglia can be divided into either lacunes or striatocapsular infarctions by size of lesion. However, there are some controversies concerning the size criteria of lacune and striatocapsular infarction. To better understand differences among these patients, we elucidated clinical and other properties of deep small basal ganglia infarctions (DSBIs), which could not be clearly classified as either lacunes or striatocapsular infarction by their sizes only. METHODS: We analyzed 27 patients with acute ischemic lesion of basal ganglia with which the size varying from 1.5 cm to 3 cm in their maximal diameters. We assessed clinical features, laboratory data, stroke risk factors, and radiologic findings such as MRI and MR angiography. RESULTS: These patients could be largely divided into two distinct groups, either with or without associated cortical symptoms and signs. The most common clinical feature was motor weakness that was found in all but one patient. Sensory disturbances, altered deep tendon reflexes, and positive Babinski signs were also commonly found. Ten of the 27 patients showed cortical manifestations such as eyeball deviation, visual field defect, aphasia and neglect. Eight of the 10 patients with cortical manifestations showed MCA or ICA stenotic lesions. CONCLUSIONS: We found that many patients with 1.5 cm to 3 cm sized DSBIs could have the features of either lacune or striatocapsular infarction. Careful evaluation of clinical and radiologic findings should be performed in patients with clinically appearing lacunar syndrome in order to differentiate lacunar infarction of small vessel disease from striatocapsular infarction of other various pathophysiologies. Echocardiogram, cerebral angiogram and perfusion and diffusion MRI could be recommended for further evaluation and to better understand the pathogenesis in these patients.

The Babinski sign--a critical review.

In 1896, Josph Babinski, a French neurologist, first described the best known neurologic eponym--"the Babinski sign". This sign is characterised by dorsiflexion of the big toe, by recruitment of the extensor hallucis longus muscle, on stimulating the sole of the foot. He himself emphasised from the outset the intimate relationship between this sign and the shortening movement in other leg muscles, which forms the flexion synergy of the lower limb. The Babinski sign is not a new reflex, rather it is released as a result of breakdown of the harmonious integration of the flexion and extension component of the normal defence reflex mechanism, due to pyramidal tract dysfunction. A pathological Babinski sign should be clearly distinguished from upgoing toes that may not always be a part of the flexion synergy. This article reviews the Babinski sign in detail, focusing on the historical perspectives, role of pyramidal tract dysfunction, art of elicitation and interpretation. The significance of assessing this phenomenon in the entire leg and the clinical clues that will help to dispel the myths regarding the Babinski sign has been emphasized.