RESUMO
Tilt suppression refers to both tilting the head away from an Earth vertical axis and a reduction of an induced horizontal nystagmus. This phenomenon of reducing an induced horizontal nystagmus involves a circuitry of neurons within the vestibular nuclei and the cerebellum (collectively referred to as velocity storage) and signals from the otolith end organs. Lesions involving this circuitry can disrupt tilt suppression of induced horizontal nystagmus. We investigated the clinical value of combining the horizontal head-shaking nystagmus test with tilt suppression in 28 patients with unilateral peripheral vestibular hypofunction and 11 patients with lesions affecting the central nervous system. Each of the subjects with peripheral vestibular lesions generated an appropriately directed horizontal nystagmus after head shaking that then suppressed the induced angular slow phase velocity on average 52 ± 17.6% following tilt down of the head. In contrast, patients with central lesions had very little ability to suppress post-head-shaking nystagmus (mean 3.4 ± 56%). We recommend tilting the head after head shaking as a useful clinical test to assist in the differential diagnosis of vertiginous patients. In the case of unilateral peripheral vestibular hypofunction, head tilt suppresses the induced nystagmus via influence of the otolith organ. In the case of central pathology, the inability to suppress the nystagmus is from lesions impairing the otolith mediation on the velocity storage circuitry.
Assuntos
Cerebelo/patologia , Cabeça/fisiologia , Movimento/fisiologia , Vias Neurais/patologia , Vertigem/diagnóstico , Núcleos Vestibulares/patologia , Adulto , Idoso , Idoso de 80 Anos ou mais , Diagnóstico Diferencial , Feminino , Humanos , Masculino , Pessoa de Meia-Idade , Nistagmo Fisiológico/fisiologia , Vertigem/etiologiaRESUMO
INTRODUCTION: Antiphospholipid antibodies lupus anticoagulant (LA) and anticardiolipin antibodies (aCL) play a role in promoting arterial and venous thrombosis in several vascular territories. Acute vestibular syndromes are a common complaint in general and neurology practice. Approximately 9% of cases are due to central nervous system vestibular areas lesions, often associated with vascular disorders. OBJECTIVE: Define the potential relationship between these antibodies and central or peripheral vestibular failure. PATIENTS AND METHODS: We report the presence of antiphospholipid antibodies in 16 patients with central vestibular symptoms. All patients were seen in the Neuro otology and Vascular Neurology clinics at the Institute for Neurological Research in Buenos Aires. Magnetic resonance imaging (MRI) and ancillary neuro otologic tests were used to determine the etiology of vestibular manifestations. Determinations of LA and aCL were done using standard criteria. RESULTS: We evaluated 16 patients (13 women and 3 men), aged 44 4 years (21 65). Thirteen patients did not have stroke risk factors. MRI lesions were found in 11 subjects (1 cerebellar infarct, 3 pontine ischemic changes, and 9 white matter abnormalities). All patients had signs consistent with dysfunction of vestibulo cerebellar structures or the vestibular nuclei. All patients had positive LA and 4 of them had also elevated aCL. CONCLUSION: Our findings suggest a potential association between the presence of a prothrombotic state and central vestibular dysfunction of vascular etiology. To the best of our knowledge, this is the first report of such an association in the absence of clinically evident autoimmune disease.
Assuntos
Anticorpos Antifosfolipídeos/metabolismo , Doenças Vasculares/imunologia , Doenças Vestibulares/imunologia , Núcleos Vestibulares/patologia , Adulto , Idoso , Anticorpos Anticardiolipina/metabolismo , Feminino , Humanos , Inibidor de Coagulação do Lúpus/metabolismo , Imageamento por Ressonância Magnética , Masculino , Pessoa de Meia-Idade , Fatores de Risco , Doenças Vasculares/patologia , Doenças Vestibulares/patologiaRESUMO
"Mal seco" is a disease of unknown aetiology affecting horses in Argentina. It is similar to grass sickness, a primary dysautonomia of horses in Europe. A histopathological study of the brain stem nuclei of three horses with "mal seco" was performed. Changes were found that consisted of chromatolysis, cytoplasmic vacuoles, eosinophilic sphaeroids, and pyknotic and eccentric nuclei. These changes were most severe at the oculomotor, vestibular and abducent nuclei. The results provide further evidence to suggest that "mal seco" and grass sickness may be the same disease.
Assuntos
Doenças do Sistema Nervoso Autônomo/veterinária , Tronco Encefálico/patologia , Doenças dos Cavalos/patologia , Animais , Doenças do Sistema Nervoso Autônomo/patologia , Feminino , Cavalos , Masculino , Neurônios/ultraestrutura , Núcleo Rubro/patologia , Núcleos Vestibulares/patologiaRESUMO
This study demonstrates that somatostatin (SRIF), an endogenous peptide in vestibular nuclei and cerebellum, can produce both a dose-dependent death of Purkinje cells in distinct sagittal regions of cerebellar cortex and vascular infarcts centered selectively in the inferior vestibular nucleus. Alert, adult male rats were given a 5 microliters intracerebroventricular (i.c.v.) bolus of either SRIF alone (20 or 40 micrograms) or a combined dose of SRIF plus either arginine-vasopressin (AVP, 1 micrograms) or an AVP V1 antagonist, (1-(beta-mercapto-beta,beta-cyclopentamethylene propionic acid), 2-(O-methyl)-tyrosine)-arginine 8-vasopressin (mcAVP, 1 micrograms), through an implanted cannula. After a 4-5 day survival, the brains were stained with the cupric-silver selective degeneration method. Two types of dose-dependent lesions were observed in the cerebellar and vestibular nuclei of these animals: degeneration of Purkinje cell responses in the cerebellar cortex and vascular infarcts in vestibular nuclei. These toxic responses were unaffected by application of AVP or mcAVP; hence, they can be attributed to actions of SRIF. The distribution of Purkinje cell degeneration varied with the SRIF dose in different cerebellar regions. Purkinje cell responses in lobules I-III were equivalent at both SRIF doses, and degeneration in the copula pyramis, paraflocculus and paramedian lobule emerged at the higher SRIF dose. Purkinje cells in the medial aspect of lobules IX-X had an intermediate sensitivity to SRIF intoxication. Degenerating Purkinje cells tended to be arranged in parasagittal bands in each region, suggesting parasagittal zonal variations in susceptibility to SRIF intoxication. By contrast, infarctions in the vestibular nuclei only appeared at the higher SRIF dose. These infarcts could be unilateral or bilateral and always involved the inferior vestibular nucleus at the level of the caudal margin of the acoustic tubercle; they often extended into the medial and lateral vestibular nuclei. The infarcts had a necrotic core that was infiltrated by non-neuronal elements. Thus, they appear to reflect a direct or neurally-mediated vascular response to the peptide.