Elettrocortical spectral analysis and fractal methods for assessing the effects of unilateral brain injury on rat cerebellum

2017 ◽  
Vol 154 (4) ◽  
pp. 118-124
Author(s):  
Ljiljana Martac
2005 ◽  
Vol 15 ◽  
pp. S245
Author(s):  
G. Grbic ◽  
Lj. Martac ◽  
M. Culic ◽  
V. Todorovic ◽  
O. Mitrovic ◽  
...  

1955 ◽  
Vol 48 (6) ◽  
pp. 478-481 ◽  
Author(s):  
Lila Ghent ◽  
Sidney Weinstein ◽  
Josephine Semmes ◽  
Hans-Lukas Teuber

Neurology ◽  
2016 ◽  
Vol 88 (2) ◽  
pp. 160-163 ◽  
Author(s):  
Ilaria Zivi ◽  
Eugenio Bertelli ◽  
Giacinta Bilotti ◽  
Ignazio Alessandro Clemente ◽  
Leopold Saltuari ◽  
...  

Objective:To describe a rare sign of unilateral brain injury as a form of unwanted blink-associated contralateral eccentric saccades.Methods:A 62-year-old patient who underwent an ischemic stroke affecting the entire right middle cerebral artery territory came to our attention 1 year after stroke, manifesting with transient contralateral conjugate gaze deviations associated with spontaneous blinking. We complemented the regular neurologic evaluation with brain MRI, study of evoked potentials, electroneurography of the facial nerve, and infrared video-oculoscopy.Results:The patient had left-sided hemiparesis, hypoesthesia, hemianopia, and hemispatial neglect. He also showed the occurrence of a rapid leftward conjugate deviation of the eyes, followed by a corrective movement to the primary ocular position. MRI showed a wide malacic area spanning the right frontal, temporal, and parietal cortical and subcortical regions, with signs of wallerian degeneration of the descending right corticospinal tract. Motor and somatosensory evoked potentials were centrally altered on the right side. Electroneurography of the facial nerves was normal. Infrared video-oculoscopy indicated persistence of the same blink-related saccades even in darkness.Conclusions:It is known that unilateral cerebral lesions may manifest with a contralateral conjugate gaze deviation evoked by closure of the lids. This sign, known as spasticity of conjugate gaze, may be due to the suppression of the fixation reflex. In our case, the persistence of this sign in the darkness allowed us to exclude this diagnosis. We hypothesized that the blink-related neural pathways may improperly activate the oculomotor circuitry at both the cortical and subcortical levels.


1992 ◽  
Vol 42 (1) ◽  
pp. 89-102 ◽  
Author(s):  
Heidi M. Feldman ◽  
Audrey L. Holland ◽  
Susan S. Kemp ◽  
Janine E. Janosky

1979 ◽  
Vol 32 (2) ◽  
pp. 535-541 ◽  
Author(s):  
M. Rigoulet ◽  
B. Guerin ◽  
F. Cohadon ◽  
M. Vandendreissche

2019 ◽  
Vol 73 (4_Supplement_1) ◽  
pp. 7311515373p1
Author(s):  
Ka Lai Au ◽  
Julie Knitter ◽  
Susan Morrow-McGinty ◽  
Talita Campos ◽  
Jason Carmel ◽  
...  

2017 ◽  
Vol 71 (4_Supplement_1) ◽  
pp. 7111515232p1
Author(s):  
Ka Lai Kelly Au ◽  
Julie L. Knitter ◽  
Susan Morrow-McGinty ◽  
Jason B. Carmel ◽  
Kathleen M. Friel

Biomeditsina ◽  
2019 ◽  
pp. 107-120
Author(s):  
Yu. I. Sysoev ◽  
K. A. Kroshkina ◽  
V. A. P’yankova ◽  
V. E. Karev ◽  
S. V. Okovitiy

A series of amplitude and spectral studies was performed to investigate brain cortical activity in rats with traumatized brain (open penetrating traumatic brain injury (TBI)). Electrocorticograms (ECoG) were recorded on the 3rd and the 7th day following the trauma. An amplitude analysis comprised an estimation of the mean signal amplitude and the degree of Lempel — Ziv compression. A spectral analysis involved a calculation of the mean amplitude and δ-, θ-, α- and β-rhythm indices. Characteristic changes in the ECoG amplitude and spectral parameters were revealed in TBI rats. Traumatized animals demonstrated decreased values of both the mean signal amplitude, as well as the amplitudes and indices of θ-, α- and β-rhythms. At the same time, the mean amplitude and the index of delta-frequency were increased. Similar changes were observed not only near the traumatized area but also in the other brain cortex regions on the 3rd and 7th day following the trauma. The obtained results demonstrate that the investigated TBI model has numerous electro physiological similarities with traumas in clinical practice, thus being applicable for neurophysiological and pharmacological studies.


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