RESUMO
The driving performance of patients with dizziness and vertigo has gained only minor attention so far. Patients with permanent vestibular loss or with episodic vestibular symptoms can experience difficulties in driving a motor vehicle. The presence of a chronic or episodic syndrome presenting with dizziness and/or vertigo does not automatically exclude the ability to drive. Assessment of driving performance should consider the degree of the deficits and compensation in chronic dysfunction and the severity and frequency of attacks, prodromes and triggers of symptoms in episodic disorders.
Assuntos
Exame para Habilitação de Motoristas/legislação & jurisprudência , Técnicas de Diagnóstico Neurológico/normas , Avaliação da Deficiência , Tontura/diagnóstico , Vertigem/diagnóstico , Alemanha , Regulamentação Governamental , HumanosAssuntos
Síndrome Medular Lateral/diagnóstico , Ilusões Ópticas/fisiologia , Orientação/fisiologia , Transtornos da Percepção/diagnóstico , Percepção Visual/fisiologia , Septo Interatrial , Diagnóstico Diferencial , Feminino , Forame Oval Patente/complicações , Forame Oval Patente/diagnóstico , Aneurisma Cardíaco/complicações , Aneurisma Cardíaco/diagnóstico , Humanos , Embolia Intracraniana/diagnóstico , Angiografia por Ressonância Magnética , Imageamento por Ressonância Magnética , Pessoa de Meia-Idade , Exame Neurológico , Tomografia Computadorizada por Raios XRESUMO
Alfred Döblin studied medicine after completing his Abitur (A-levels). In 1905 he earned his doctorate under Alfred Hoche, director of the psychiatric clinic, by presenting a study on "Memory disorders in Korsakoff's psychosis." He subsequently worked as an assistant doctor in various psychiatric clinics until he switched to internal medicine in 1908. He opened a practice as panel doctor in 1911, which he operated until 1930. Although Döblin had already published a few stories, he first became generally known in 1929 with the appearance of his novel entitled "Berlin Alexanderplatz: the story of Franz Biberkopf." After the burning of the Reichstag in February 1933, as a Jewish socialist Döblin was forced to emigrate. He was unable to work as a physician during his exile, but remained active in his literary pursuits. Döblin died on 26 June 1957 in the state hospital in Emmendingen.
Assuntos
Literatura Moderna/história , Psiquiatria/história , Alemanha , História do Século XXAssuntos
Edema Encefálico/terapia , Craniotomia , Encefalomielite Aguda Disseminada/terapia , Adulto , Encéfalo/patologia , Encéfalo/cirurgia , Edema Encefálico/complicações , Progressão da Doença , Encefalomielite Aguda Disseminada/complicações , Encefalomielite Aguda Disseminada/diagnóstico , Feminino , Glucocorticoides/uso terapêutico , Hemiplegia/etiologia , Humanos , Imunoglobulinas Intravenosas/uso terapêutico , Pressão Intracraniana , Imageamento por Ressonância Magnética , Manitol/uso terapêutico , Metilprednisolona/uso terapêutico , Tomografia Computadorizada por Raios XRESUMO
Drug-induced ocular motor disorders occurring during coma may be difficult to distinguish from structural cerebral lesions. We recently encountered a case of reversible amitriptyline-induced external ophthalmoplegia, which was first described by Mladinich and Carlow in 1977. We suggest that the mechanism for gaze paresis and loss of vestibulo-ocular reflex due to amitriptyline overdose involves the modulation of neurons of the pontine paramedian reticular formation, the rostral fasciculus longitudinalis medialis, and the vestibulo-ocular reflex. Clinical features that might be useful when distinguishing amitriptyline-induced ophthalmoplegia from structural brain lesions--such as basilar thrombosis--include the preservation of corneal response, purposeful withdrawal from noxious stimuli, rapid recovery within 24 hours, and the reversal of symptoms by physostigmine.
Assuntos
Amitriptilina/intoxicação , Antidepressivos Tricíclicos/intoxicação , Overdose de Drogas/diagnóstico , Oftalmoplegia/induzido quimicamente , Adulto , Piscadela/efeitos dos fármacos , Transtorno Depressivo/tratamento farmacológico , Diagnóstico Diferencial , Humanos , Masculino , Oftalmoplegia/diagnóstico , Reflexo Vestíbulo-Ocular/efeitos dos fármacosAssuntos
Angioplastia com Balão , Encéfalo/irrigação sanguínea , Estenose das Carótidas/terapia , Hemorragia Cerebral/diagnóstico por imagem , Hiperemia/diagnóstico por imagem , Stents , Ultrassonografia Doppler Transcraniana , Anticoagulantes/administração & dosagem , Anticoagulantes/efeitos adversos , Estenose das Carótidas/diagnóstico por imagem , Quimioterapia Combinada , Humanos , Masculino , Pessoa de Meia-Idade , Monitorização FisiológicaRESUMO
BACKGROUND AND PURPOSE: Cerebral autosomal dominant arteriopathy with subcortical infarcts and leukencephalopathy (CADASIL) is a hereditary angiopathy caused by mutations in Notch3. Cerebral microvessels show an accumulation of granular osmiophilic material in the vicinity of degenerating vascular smooth muscle cells. To study cerebrovascular function in CADASIL, we performed measurements on cerebral hemodynamics by using transcranial Doppler sonography. METHODS: Middle cerebral artery (MCA) mean blood flow velocity (MFV), cerebrovascular CO(2) reactivity, and the resistance index were measured by bilateral transcranial Doppler sonography in 29 CADASIL individuals (mean age, 49.0+/-2.4 years) and an equal number of age- and sex-matched control subjects. RESULTS: Compared with control subjects, CO(2) reactivity was reduced in CADASIL (33.4+/-2.7% versus 45.3+/-3.0%; P:<0.01). This difference remained significant when only nondisabled CADASIL individuals (Rankin=0, n=21) were included in the analysis (P:<0.05). CO(2) reactivity was significantly lower in disabled than in nondisabled CADASIL individuals (24.5+/-2.7% versus 36.8+/-3.4%; P:<0.05). MCA MFV was reduced in CADASIL (45.6+/-2.2 cm/s versus 54.2+/-2.4 cm/s; P:<0.05) and correlated negatively with age both in affected individuals (r=-0.314; P:<0.05) and control subjects (r=-0.339; P:<0.05). Resistance index was not significantly altered (59.0+/-1.0% versus 57.7+/-1.2%; P:=0.42). CONCLUSIONS: In CADASIL, there is a reduction of both CO(2) reactivity and basal MCA MFV. The reduced CO(2) reactivity suggests functional impairment of cerebral vasoreactivity probably related to vascular smooth muscle cell dysfunction. The reduction of CO(2) reactivity in nondisabled CADASIL individuals suggests an early role of impaired cerebral vasoreactivity in the evolution of the disease.
Assuntos
Dióxido de Carbono/metabolismo , Circulação Cerebrovascular , Demência por Múltiplos Infartos/diagnóstico por imagem , Demência por Múltiplos Infartos/metabolismo , Receptores de Superfície Celular , Ultrassonografia Doppler Transcraniana , Adulto , Fatores Etários , Idoso , Idoso de 80 Anos ou mais , Velocidade do Fluxo Sanguíneo , Demência por Múltiplos Infartos/genética , Demência por Múltiplos Infartos/fisiopatologia , Feminino , Humanos , Hipercapnia/metabolismo , Hipocapnia/metabolismo , Masculino , Pessoa de Meia-Idade , Artéria Cerebral Média/diagnóstico por imagem , Músculo Liso Vascular/fisiopatologia , Proteínas Proto-Oncogênicas/genética , Receptor Notch3 , Receptores Notch , Resistência VascularRESUMO
Post-lumbar puncture headache (PLPH) is best explained by spinal fluid leakage due to delayed closure of a dural defect. In a prospective, randomized, double-blind study, taking into consideration all known methodological problems, the authors compared the incidence of PLPH using the "atraumatic" Sprotte needle vs the "traumatic" Quincke needle. Of the 230 patients included in the final analysis, 24.4% of patients in the "traumatic" group developed PLPH, whereas only 12.2% of patients in the "atraumatic" group did (p < 0.05). Therefore, use of the "atraumatic" Sprotte needle for lumbar puncture is recommended.
Assuntos
Cefaleia/etiologia , Cefaleia/fisiopatologia , Agulhas/efeitos adversos , Punção Espinal/efeitos adversos , Adulto , Feminino , Humanos , Masculino , Pessoa de Meia-IdadeRESUMO
The composition of various amino acids and related compounds in the aorta, ventricle, atria, liver, kidney, pancreas, bronchi and adrenals of rats is presented. These patterns are qualitatively similar, but quantitatively different. Stress changed these patterns. In the aorta, alpha-aminobutyric acid and ammonia are decreased. In the ventricle, phosphoserine and red. Glutathione are increased; and ammonia, arginine, asparagine, carnosine, ethanolamine, glutamic acid, glutamine, lysine, phosphoethanolamine and taurine are decreased. In the atria, alpha-aminobutyric acid, aspartic acid, ethanolamine and red. glutathione are increased; and ammonia is decreased. In the liver, alpha-aminobutyric acid, cystine, isoleucine, red. glutathione, methionine and phenylalanine are increased. In the kidney, ethanolamine is increased; and beta - aminobutyric acid, citrulline, cystathionine, glutamic acid, glycine and tryptophan are decreased. In the pancreas, alpha-aminoadipic acid, ox. glutathione, leucine, glutamine, 1-methylhistidine, phenylalanine, phosphoserine, tryptophan and valine are increased; and ammonia, cystine and aspartic acid are decreased. In the adrenal glands, anserine, glutamic acid, glutamine and ox. glutathione are increased; and arginine is decreased. In the bronchi, ethanolamine and beta-alanine are increased and alpha-aminobutyric acid and ox. glutathione are decreased. Thus, stress affects certain amino compounds but changes are substance and tissue specific and independent of changes seen in the plasma.