Bilateral occipital lobe infarct neglect deficit (BLIND) syndrome.

Cortical blindness is characterized by loss of vision due to dysfunction of the visual cortices, most commonly secondary to bilateral ischemic infarcts of the occipital lobe. Other causes include surgery such as aortic valve replacement, laryngeal surgery, craniotomy, cerebral angiography, head trauma, and partial seizures. Visual anosognosia is a distinct feature of cortical blindness, wherein patients claim they can see and confabulate visual perceptions, despite loss of sight. We herewith present a rare phenomenon known as Anton Syndrome, an eponym named after the Austrian neurologist and psychiatrist, Gabriel Anton (1858-1933). There are a limited number of cases of Anton's Syndrome in the literature, with only 28 case reports published from 1965-2016. Although he was bestowed a neurologic eponym, Anton was an advocate of eugenics and racial hygiene. He publicly advocated for 'superior breeding' and 'selection' in order to 'build a brave and noble race.' We therefore propose replacing the eponym with Bilateral Occipital Lobe Infarct Neglect Deficit (BLIND) Syndrome, with intention of raising awareness of this unique presentation as well as of the widespread interest in eugenics in the early 1900s amongst physicians, notably Gabriel Anton.

Measurement of spinal cord blood flow by the microsphere technique.

Differential spinal cord blood flow was measured in dogs by the radioactive microsphere injection method. The mean spinal cord blood flow was 10.8 +/- 0.53 (SE) ml/100 g/minute. The flow values for the white and gray matter were 7.1 +/- 0.65 (SE) and 26.3 +/- 2.2 (SE) ml/100 g/minute, respectively.

Granulomatous angiitis of the brain: a successfully treated case.

A patient with clinical and radiographic findings initially suggesting a neoplasm was diagnosed as having Hodgkin disease. Computerized axial tomography demonstrated profound diffuse decreased density similar to that seen in cases of cerebral edema or leukomalacia. Cerebral angiography showed blood vessels with a beaded appearance. A diagnosis of granulomatous angitis was made on the basis of brain biopsy specimens. Viral cultures were negative. Skin testing revealed poor response to antigens. The patient improved dramatically following a combination of radiotherapy and steroid therapy. Resolution of the low-density abnormally seen on serial EMI scanning and resolution of the vasculitis demonstrated in the post-therapy brain biopsy specimen was dramatic. This is the first case of granulomatous angitis of the brain diagnosed during life, and it points out the value of radiation and steroid therapy for relief of neurologic symptoms.

Demonstration of massive traumatic brain swelling within 20 minutes after injury. Case report.

The authors documented by computerized axial tomography a case of massive brain swelling occurring within 20 minutes of a closed head injury. It is suggested that the cause of the brain swelling is acute vascular dilatation.

Hodgkin's disease and granulomatous angiitis of the central nervous system.

Granulomatous angiitis of the central nervous system, a pathologic entity associated previously with a fatal prognosis, is reported in a patient with Hodgkin's disease. Viral isolation, indirect fluorescent antibody, and electron microscopic studies performed on fresh cerebral tissue were negative. The granulomatous angiitis of the central nervous system in this patient remitted following therapy for Hodgkin's disease. The epidemiologic, clinical and pathologic data in all reported cases of granulomatous angiitis of the central nervous system suggest that it: 1) may have more than one etiology; 2) may not always be fatal; 3) is associated with varicella-zoster virus and Hodgkin's disease; 4) is one of two granulomatous reactions found in association with Hodgkin's disease; and when found with Hodgkin's disease, 5) may remit with adequate therapy for the lymphoma.

Significance of Purkinje cell density in seizure suppresion by chronic cerebellar stimulation.

Cerebellar biopsy specimens were obtained at the time of cerebellar electrode installation in three epileptic patients. Cerebellar autopsy specimens also were examined from four epileptic patients and from five patients without epilepsy or neurologic disease. All specimens from seizure patients showed isomorphic gliosis of the cerebellar cortices. Significantly lower Purkinje cell densities were found in epileptic patients as compared with nonepileptic control patients. Our two epileptic patients showing marked Purkinje cell loss before cerebellar stimualtaion appeared to have better seizure control during stimulation than the patient who had only mild reduction in Purkinje cell density. These data suggest that augmentation of Purkinje cell inhibitory discharges in not the dominant mechanism for seizure suppression during cerebellar stimulation. Comparison of cerebellar specimens obtained during electrode installation with those obtained later during electrode revisions may have been prognostic significance.