scholarly journals Downbeat Nystagmus Secondary to Chiari I Malformation

2021 ◽  
Author(s):  
Marcelo Tognato Ximenes ◽  
Dan Mohamed Salman ◽  
Francisco Tomaz Meneses de Oliveira ◽  
Rubens José Gagliardi
Keyword(s):  
Chiari I Malformation ◽  
Moderate Intensity ◽  
Downbeat Nystagmus ◽  
Lateral Instability ◽  
Rapid Phase ◽  
Primary Position ◽  
Chiari Type 1 Malformation ◽  
Subcortical Region ◽  
Acute Changes ◽  
The Right

Context: Downbeat nystagmus are characterized by the rapid phase in the down direction in primary position of the eyes, in the most cases represents a cerebellar dysfunction, typically with injuries involving vestibulocerebellum (flocculus, paraflocculus, nodule and uvula), although most cases are due to primary lesions in the brain stem, usually involving paramedian tracts. This type of nystagmus is characteristic of craniocervical abnormalities, such as Chiari 1 malformation, also being seen in a wide variety of cerebellar diseases, including degenerative etiologies, toxic-metabolic and ischemic injury. Case report: A 45-year-old woman, who presented with dizziness started 6 years ago, related to rapid head movement, with progressive worsening, leading to difficulty in walking and a tendency to fall to the right, associated with mild to moderate intensity occipitonuchal headache, with improvement at rest and horizontal decubitus. Neurological examination showed downbeat nystagmus, intent tremor in the finger-to-nose-test, worse on the right arm, Romberg test presentes with anteroposterior and lateral instability, in addition to Tanden with bilateral lateropulsion, without other relevant changes. The magnetic resonance imaging showed platybasia and vertebrobasilar invagination, Chiari type 1 malformation with tonsillar herniation, without signs of cervical hydrosyringomyelia, signs of atrophy of both cerebellar hemispheres, a nonspecific nodule in the subcortical region of the left precuncle. Conclusion: The case described above is relevant to demonstrate that even in cases of acute changes in adulthood, screening for anatomical malformations in the posterior fossa should be considered.

scholarly journals Anti-Ma-associated paraneoplastic cerebellar degeneration in a patient with nodular lymphocyte-predominant Hodgkin lymphoma: a case report

BMC Neurology ◽  
2020 ◽  
Vol 20 (1) ◽  
Author(s):  
Ryoma Inui ◽  
Kenki Saito ◽  
Yoshimitsu Shimomura ◽  
Daisuke Yamashita ◽  
Michi Kawamoto ◽  
...  
Keyword(s):  
Lymph Node ◽  
Hodgkin Lymphoma ◽  
Paraneoplastic Syndrome ◽  
Cerebellar Degeneration ◽  
Paraneoplastic Cerebellar Degeneration ◽  
Downbeat Nystagmus ◽  
Primary Position ◽  
First Case ◽  
History Of ◽  
The Right

Abstract Background Paraneoplastic cerebellar degeneration (PCD) is a devastating paraneoplastic syndrome that occasionally occurs in patients with Hodgkin lymphoma (HL). Anti-Ma2 is a well-characterized onconeuronal antibody and one of the causes of PCD. There has been only one previous report of anti-Ma2-associated paraneoplastic syndrome as a complication of HL. Here we present a rare case of anti-Ma2-associated PCD in a patient with nodular lymphocyte-predominant HL (NLPHL). Case presentation A 77-year-old man with a 3-month history of gait instability and a 2-month history of oscillopsia was referred to our hospital for further investigation. On examination, his cognition was normal. He had nystagmus in all directions of gaze; specifically, he had horizontal and rotatory nystagmus in the primary position, downbeat nystagmus after right, left, and up gaze, and upbeat nystagmus after down gaze. Although his limb ataxia was mild, his trunk ataxia was so pronounced that he was unable to walk without support. We strongly suspected paraneoplastic syndrome and tested for neuronal autoantibodies. The anti-Ma2 antibody was strongly positive in the blood and cerebrospinal fluid but other antineuronal autoantibodies were negative. Computed tomography showed an enlarged lymph node in the right axilla but no masses. Biopsy confirmed a diagnosis of NLPHL. The NLPHL cells stained with anti-Ma-2 antibody in the cytoplasm, suggesting these abnormal cells contained protein that was cross-reactive with Ma-2. Conclusions To the best of our knowledge, this is the first case of anti-Ma2-associated PCD in a patient with NLPHL that was confirmed using immunostaining of the lymph node tissue with anti-Ma2 antibody. Our case confirms an association between anti-Ma2-associated PCD and NLPHL.

Blow/trauma to the chest and sudden cardiac death: Commotio cordis and contusio cordis are leading causes

2018 ◽  
Vol 58 (2) ◽  
pp. 93-96 ◽  
Author(s):  
Lydia Krexi ◽  
Mary N Sheppard
Keyword(s):  
Sudden Cardiac Death ◽  
Cardiac Death ◽  
Traffic Accidents ◽  
Left Ventricular ◽  
Young Males ◽  
Contusio Cordis ◽  
Commotio Cordis ◽  
Forensic Practice ◽  
Acute Changes ◽  
The Right

Background In forensic practice, a blow to the chest can lead to sudden cardiac death (SCD). Commotio cordis and contusio cordis are leading causes. Methods From a database of 4678 patients who suffered from SCD, we found three patients with commotio cordis and two patients with contusio cordis. All the patients were examined macroscopically and microscopically and had negative toxicology screen. Results The three patients who died due to commotio cordis were young males (16, 23 and 38 years old). The circumstances of death were: a blow to the chest by a football, by a friend during a party and during an assault. The hearts were completely normal at autopsy. The two patients who had contusio cordis were older males (42 and 63 years old). Both patients died during traffic accidents. At autopsy, one had significant contusion over the left ventricle, and the second had contusion over the right ventricle. Conclusion This study indicates that a blow to the chest is very important to document in the circumstances of death, and a detailed history is vital. It raises the left ventricular intra-cavitary pressure, leading to commotio cordis with immediate death with a normal heart. Blunt chest trauma can cause direct myocardial lesions, with acute changes leading to contusio cordis.

scholarly journals Cyclic GMP regulates activation of phosphoinositidase C by bradykinin in sensory neurons

1996 ◽  
Vol 316 (2) ◽  
pp. 539-544 ◽  
Author(s):  
Justine S. HARVEY ◽  
Gillian M. BURGESS
Keyword(s):  
Cyclic Gmp ◽  
Inhibitory Effect ◽  
Neonatal Rat ◽  
Drg Neurons ◽  
Rapid Phase ◽  
Surface Receptors ◽  
Similar Inhibitory Effect ◽  
Key Factor ◽  
The Right ◽  
Oxide Synthase

Prior exposure of cultured neonatal rat dorsal root ganglion (DRG) neurons to bradykinin resulted in marked attenuation of bradykinin-induced activation of phosphoinositidase C (PIC). The (logconcentration)–response curve for bradykinin-induced [3H]inositol trisphosphate ([3H]IP3) formation was shifted to the right and the maximum response was reduced. Bradykinin increases cyclic GMP (cGMP) in DRG neurons [Burgess, Mullaney, McNeill, Coote, Minhas and Wood (1989) J. Neurochem. 53, 1212–1218] and treatment of the neurons with dibutyryl cGMP (dbcGMP) had a similar, inhibitory, effect on bradykinin-induced [3H]IP3 formation. NG-Nitro-L-arginine (LNNA) blocked bradykinin-induced formation of cGMP. It prevented the functional uncoupling induced by pretreatment with bradykinin, but not the inhibitory effect of dbcGMP on [3H]IP3 formation. The ability of LNNA to prevent desensitization was reversed by excess L-arginine, indicating that its actions were mediated through inhibition of nitric oxide synthase. In addition to functional desensitization, exposure to bradykinin reduced the number of cell-surface receptors detected with [3H]bradykinin, without affecting its KD value for the remaining sites. In contrast to bradykinin, pretreatment with dbcGMP had no effect on either the KD or Bmax for [3H]bradykinin binding. This implies that the inhibitory effect of dbcGMP was downstream from the binding of bradykinin to its receptor and upstream of IP3 formation. The lack of effect of dbcGMP on [3H]bradykinin binding suggests that the decrease in receptor number induced by bradykinin was mediated by a different mechanism and was not a key factor in the rapid phase of desensitization in these cells.

scholarly journals Persistent Upbeat Positional Nystagmus in a Patient with Bilateral Posterior Canal Benign Paroxysmal Positional Vertigo

2019 ◽  
Vol 2019 ◽  
pp. 1-3
Author(s):  
Akihide Ichimura ◽  
Shigeto Itani
Keyword(s):  
Supine Position ◽  
Benign Paroxysmal Positional Vertigo ◽  
Semicircular Canals ◽  
Downbeat Nystagmus ◽  
Positional Vertigo ◽  
Head Roll ◽  
The Right ◽  
Upbeat Nystagmus ◽  
Torsional Nystagmus ◽  
Paroxysmal Positional Vertigo

Here, we report a patient with persistent positional upbeat nystagmus in a straight supine position with no evident abnormal central nervous system findings. A 43-year-old woman with rotatory positional vertigo and nausea visited our clinic 7 days after the onset. Initially, we observed persistent upbeat nystagmus in straight supine position with a latency of 2 s during the supine head roll test. However, an upbeat nystagmus disappeared on turning from straight to the left ear-down supine position, and while turning from the left to right ear-down position, an induced slight torsional nystagmus towards the right for >22 s was observed. In the Dix–Hallpike test, the left head-hanging position provoked torsional nystagmus towards the right for 50 s. In prone seated position, downbeat nystagmus with torsional component towards the left was observed for 45 s. Neurological examination and brain computed tomography revealed no abnormal findings. We speculated that persistent positional upbeat nystagmus in this patient was the result of canalolithiasis of benign paroxysmal positional vertigo of bilateral posterior semicircular canals.

Assessment of the MyWellness Key accelerometer in people with type 2 diabetes

2015 ◽  
Vol 40 (11) ◽  
pp. 1193-1198 ◽  
Author(s):  
Samantha Kate McGinley ◽  
Marni J. Armstrong ◽  
Farah Khandwala ◽  
Silvano Zanuso ◽  
Ronald J. Sigal
Keyword(s):  
Type 2 Diabetes ◽  
Normal Weight ◽  
Moderate Intensity ◽  
Exercise Session ◽  
Free Living ◽  
The Mean ◽  
Moderate Intensity Activity ◽  
The Right ◽  
Treadmill Protocol

Accelerometers are designed to measure physical activity (PA) objectively. The MyWellness Key (MWK) accelerometer has been validated primarily in younger, normal-weight populations. The aims of this study were to examine the accuracy of the MWK against directly measured lab-based exercise and free-living PA in people with type 2 diabetes, many of whom are older and overweight or obese. Thirty-five participants with type 2 diabetes completed the protocol, which included a laboratory-based session and a free-living phase. In the laboratory visit, participants completed a structured treadmill protocol wearing MWKs on each hip (all subjects) and bra cup (women only). The speed where each MWK switched from recording light- to moderate-intensity activity was determined for each MWK worn. In the free-living phase, participants wore the MWK for all waking hours for 2 weeks, and recorded exercise in PA diaries immediately after each exercise session. The mean cut-points between low (“Free”) and moderate (“Play”) intensity for the right and left waist-worn MWKs were 4.1 ± 0.5 km/h and 5.0 ± 0.9 km/h for the bra-mounted MWK; ideal cut-point would be 4.0 km/h. In the free-living phase, the Spearman correlation between PA according to PA diary and the waist-worn MWK was 0.81 (95% confidence interval (CI): 0.76, 0.85; P < 0.001), but only 0.66 (95% CI: 0.53, 0.77; P < 0.001) when on the bra. In conclusion, the waist-worn MWK measured PA volume accurately, and was acceptably accurate at discriminating between low- and moderate-intensity PA in people with type 2 diabetes. The MWK underestimated PA volume and intensity when worn on a bra.

*Siringomielia asociada a Malformación de Chiari I. Reporte de caso. [Syringomyelia associated with Chiari I Malformation. Case report.]

2021 ◽  
Vol 40 (03) ◽  
Author(s):  
Flor Wilson Giraldo ◽  
Hector Lezcano ◽  
Leonardo Barrios
Keyword(s):  
Cranial Nerves ◽  
Chiari I Malformation ◽  
Clinical Suspicion ◽  
Unknown Etiology ◽  
Type I ◽  
Imaging Studies ◽  
Structural Alterations ◽  
Truncal Ataxia ◽  
Chiari I ◽  
The Right

<p>Introducción: Las Malformaciones de Chiari (M.C.) son alteraciones estructurales a nivel del cerebelo de etiología en estudio. Muy raras, afectan al 0,5% de la población. Más de la mitad de los pacientes cursan con siringomielia. Caso clínico: Femenina de 47 años con antecedente de M.C. Tipo I, acude con cuadro de dos semanas de evolución de cefalea holocraneana de intensidad 8/10, asociado a mareo e inestabilidad a la marcha. Hallazgos positivos de alteración en los pares craneales III, VIII, IX; hipertonía, signo de Babinski y Hoffman positivos bilaterales; ataxia truncal; nistagmus a la derecha; fuerza muscular disminuida en miembros superiores e hiperreflexia. Discusión: Ante la sospecha clínica, y las múltiples alteraciones a nivel del cerebelo y bulbo, se procede a realizar estudios de imagen y se confirma el diagnóstico de siringomielia.</p><p><strong>Abstract: </strong></p><p>Introduction: Chiari malformations (C.M.) are structural alterations in cerebellum. They are of unknown etiology, at present in study. They are very rare and affect 0,5 % of the population. More than half of the patients have syringomyelia. Clinical case: A 47-year-old female with medical record of C.M. Type I, presents with a two-week evolution holocranial headache, 8/10 in intensity, associated with dizziness and gait instability. Positive findings of alteration in cranial nerves III, VIII, IX; hypertonia, Babinski and Hoffman bilateral sign; truncal ataxia; nystagmus on the right; decreased muscle strength in the upper limbs and hyperreflexia. Discussion: Due to clinical suspicion and multiple alterations in cerebellum and bulb, imaging studies are performed and the diagnosis of syringomyelia is confirmed.</p>

scholarly journals P269 When sudden cardiac death is the first symptom

2020 ◽  
Vol 21 (Supplement_1) ◽  
Author(s):  
J Abdala Lizarraga ◽  
S Sanchez Alvarez ◽  
P Garcia Gonzalez ◽  
B Trejo Velasco ◽  
V Vidal Urrutia ◽  
...  
Keyword(s):  
Cardiac Arrest ◽  
Coronary Artery ◽  
Physical Exercise ◽  
Left Main Coronary Artery ◽  
Sudden Cardiac Arrest ◽  
Anomalous Origin ◽  
Moderate Intensity ◽  
Sinus Of Valsalva ◽  
Left Main ◽  
The Right

Abstract A 43-year-old male was brought to the emergency department due to a recovered sudden cardiac arrest that occurred while performing physical exercise of moderate intensity. The patient was admitted in a coronary care unit and performed complementary tests to rule out immediate causes of cardiac arrest electrocardiogram showed sinus rhythm, no repolarization abnormalities and normal QTc interval. Echocardiogram revealed no evidence of cardiac tamponade, massive pulmonary embolism (PE), ventricular dysfunction or valvular heart disease. Absence of pneumothorax in chest X-ray. Arterial blood gas test revealed a high lactate concentration with other parameters in normal range. Cerebral tomography showed absence of an acute hemorrhagic event. To continue with the study an emergent coronarography was performed showing epicardial arteries with no significant obstructive coronary artery disease associated with an anomalous origin of left main coronary artery in the right sinus of Valsalva with possible interarterial course. Coronary tomography confirmed the origin of the right coronary artery and the left main coronary artery in the right sinus of Valsalva with an interarterial course, proceeding to the reconstruction of the images with the volume rendering (VR) technique (Figure 1). Congenital anomalies of the coronary arteries are a rare but life-threatening condition. Most coronary abnormalities are asymptomatic and follow a benign course, however, in some cases they present with ischemic symptoms, heart failure, myocardial infarction, syncope or sudden death. The anomalous origin of the left main coronary artery in the right sinus of Valsalva can cause myocardial ischemia and should be ruled out in young patients who present sudden cardiac arrest induced by physical exercise. Abstract P269 Figure 1

Effect of caval occlusion on the magnitude of unipolar atrial electrograms in dogs

1983 ◽  
Vol 245 (4) ◽  
pp. H580-H583
Author(s):  
R. A. Bedont ◽  
J. A. Abildskov ◽  
R. L. Lux ◽  
L. S. Green
Keyword(s):  
Right Atrium ◽  
Superior Vena ◽  
Vena Cava ◽  
P Wave ◽  
Radial Excitation ◽  
Heart Volume ◽  
Atrial Electrograms ◽  
Acute Changes ◽  
The Right ◽  
Brody Effect

Studies were done on eight mongrel dogs anesthetized with pentobarbital sodium to assess the effects of acute changes in heart volume on the magnitude of electrocardiographic potentials recorded from the right atrium. Following midsternotomy, acute changes in heart volume were produced by occlusion of the superior vena cava (SVC), inferior vena cava (IVC), or both vena cavae while heart rate was controlled by pacing the right atrium. P-wave area, defined by integrating absolute value of the P wave over time, increased by 8.2 +/- 7.4% during SVC occlusion, 13.3 +/- 8.5% during IVC occlusion, and 23.6 +/- 16.2% during occlusion of both vena cavae. Areas of ventricular complexes appearing in atrial electrograms decreased by 6.6 +/- 6.2% during SVC occlusion, 11.1 +/- 6.7% during IVC occlusion, and 15.2 +/- 9.2% during occlusion of both vena cavae. These results are compatible with predominately tangential activation of the atrium and radial excitation of the ventricle and provide experimental confirmation of the "Brody effect."

Chiari malformation with syringocephaly

1991 ◽  
Vol 75 (5) ◽  
pp. 791-794 ◽  
Author(s):  
Eric L. Rhoton ◽  
Albert L. Rhoton
Keyword(s):  
Chiari Malformation ◽  
Mass Effect ◽  
Chiari I Malformation ◽  
Cerebral Peduncle ◽  
Content Type ◽  
Suboccipital Craniectomy ◽  
Root Entry Zone ◽  
Dural Graft ◽  
Upper Cervical ◽  
The Right

✓ A 69-year-old white woman presented with a left hemiparesis which progressed to quadriparesis and encephalopathy. Computerized tomography and magnetic resonance imaging revealed a Chiari I malformation and a hydromyelic cavity extending from C-2 to T-6. Rostrally, the cavity extended through the ventral medulla, pons, and right cerebral peduncle into the right cerebral hemisphere, where the cavity enlarged and was associated with mass effect. The patient has made a dramatic neurological recovery following suboccipital craniectomy with insertion of a dural graft to decompress the Chiari malformation and upper cervical laminectomy and dorsal root entry zone myelotomy to decompress the hydromyelia.

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