Two syndromatic forms of Creutzfeldt-Jakob disease are illustrated with data from two cases confirmed by necropsy and studied by means of electroencephalogram, evoked potential recording and neuropathological techniques. One of the cases presented the typical hypersynchronous periodic discharges through to be characteristic of this disease. The other did not exhibit epileptiform discharges, showing an evolution in which progressive diffuse slowing was the prominent feature. Cortical spongyosis, gliosis, and neuronal lose were intense in the case showing spikes, and moderate in the one without spikes. Subcortical involvement was similar in both cases. This different topography of pathological involvement might explain, in addition to electroencephalographic findings, the different behavior of somatosensory evoked potentials, which were of larger amplitude in the case showing epileptiform discharges, although in both cases deterioration of clinical state was accompanied by a progressive amplitude decrement in the evoked potential. Sleep induced by barbiturates was disrupted in the case with spikes, its pattern being closer to normal in the case with less severe cortical involvement. A Wada test demonstrated that discharges in the hemispheres were independent. Spike periodicity is discussed. It is postulated that the heavier involvement of cortical layers II to IV deprive the remaining pyramidal cells of inhibitory influences, a condition which might explain the generation of periodic spike discharges.
Arteritis de células gigantes en el sistema vertebrobasilar, isquemias cerebelo-occipitales y parálisis III par. Caso clínico adolFo del Canto a. 1,2 , FranCisCa Montoya s. 3 , roberto Marileo z. 3 , luis Cartier r. 1,2Giant cell arteritis of the vertebrobasilar system, posterior ischemia and palsy of the third nerve. Report of one case Giant cell arteritis is the most common vasculitis in patients aged over 50 years. We report an 89-year-old woman with significant weight loss and persistent frontal-occipital headaches lasting two months. The neurological examination at admission identified a decrease in visual acuity of the left eye, paralysis of the third cranial nerve of the right eye and alterations of body motility without objective signs of damage of the motor or sensitive pathways. Magnetic resonance imaging showed changes of the temporal artery wall and in both vertebral arteries, as well as bilateral cerebellar and occipital ischemic lesions. The Doppler ultrasound of the temporal arteries was compatible with Giant cell arteritis. Treatment with steroids was started. While receiving oral prednisone, the patient suffered new infarcts of the posterior territory, documented with a CAT scan. (Rev Med Chile 2018; 146: 1356-1360
Background: Lymphotropic Virus Type I (HTLV-I) causes Tropical Spastic Paraparesis (PET) in 3% of infected patients; in whom have been described exceptionally associated a central vestibular syndrome and cerebellar atrophy. Those alterations of CNS are predominating in women. Purpose: To present a new case of the exceptional form of spastic paraparesis and cerebellar atrophy. To suggest a pathogenic interpretation of female predominance in this pathology Patient: A 20-year-old woman of small size, infected with HTLV-I during lactation. Approximately at 15 years of age he started a progressive ataxo-spastic syndrome, later cognitive damage and cerebellar atrophy were added. Upon admission, high viral load and high levels of Tax protein, leukemoid lymphocytes and Sicca syndrome were observed. Conclusion: PET is an axonopathy of the central motor pathway, originated by a chronic disturbance of axoplasmic transport, attributable to the action of elevated levels of Tax protein in the CNS. In addition axons of the oval center (cognitive impairment) or the cerebellar vermis (central vestibular syndrome) are occasionally damaged. Although PET mainly affects 3: 1 women, this prevalence increases in accordance with the increase of neurological damage. The apparent greater vulnerability of the CNS in women would be due to the higher concentration of Tax in the CNS of them, originated in the adverse relationship between body weight and absolute amount of Tax, which was evident in our patient, who gave the key to this hypothesis.
Cerebral ptosis. Analysis of six cases Background: Cerebral ptosis is understood as the bilateral paralysis of eyelid elevation linked to a stroke or hemorrhage of the middle cerebral artery (MCA). It is a transient condition, independent of the evolution of the lesion. Aim: To analyze six patients with the condition. Patients and Methods: Report of five women and one male aged 42 to 72 years. Results: All suffered an infarction or hemorrhage in the territory of the middle cerebral artery of the non-dominant hemisphere and developed a bilateral palpebral ptosis. The recovery started after the fourth day. At the tenth day, eye opening was effortless and did not require frontal help, despite the persistence of hemiplegia. Conclusions: Cerebral ptosis is a mimetic dysfunction of a specific non-injured area of the cerebral cortex, originated from a nearby parenchymal damage such as the middle cerebral artery of the same hemisphere. Cerebral ptosis expresses the inhibition of the voluntary eyelid elevation center, of prefrontal location in the non-dominant hemisphere.
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