Topamax - A Medical Dictionary, Bibliography, and Annotated Research Guide to Internet References
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He denied any history of neurological symptoms in past. Case Description: MRI brain on admission showed isolated corpus callosum hyperintensity.
Cerebral spinal fluid CSF studies were significant for oligo clonal bands, elevated proteins and IgG immune globulins. IV steroids were started, clinical features though continued to progress with repeat MRI brain imaging at 1 week showing enlargement of corpus callosum lesion with further extension towards left parietal lobe.
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PET scan imaging did not show any abnormal uptake. Extensive CSF and serological studies were sent to Mayo clinic for further studies. Demyelinating disease process was suspected. Plasmapheresis was initiated for patient's progressive clinical and radiological findings. At the end of his plasmapheresis treatments, he showed clinical improvement with no further radiological progression confirmed by repeat MRI brain study at the end of plasmapheresis treatments. Patient was discharged to inpatient rehabilitation. MAID is an autoimmune response that could be triggered by an infectious disease or vaccine.
In this case albuminocytologic dissociation and oligoclonal bands were noted in CSF, and patient has history of autoimmune hemolytic anemia. Some cases of MAID show improvement with a course of steroids. Others improved with plasmapheresis and administration of IVIG. Our patient responded to plasmapheresis that stopped his clinical and radiological disease progression. A definitive cure for this disease is not known.
References: Gutrecht, J. Despite its ambiguous symptomology and infrequent presentation, a detailed workup must be conducted to rule out this disorder. This patient also exhibited irritability, frequent outbursts, as well as episodic staring spells. At the time of presentation, the patient was somnolent though easily arousable.
On exam, no cranial nerve deficits were seen. Muscle strength, sensation and reflexes were intact. Initially, MRI of the brain was obtained demonstrating diffuse leptomeningeal thickening and enhancement, alongside scattered nodular enhancement within the left medial temporal lobe.
CSF analysis demonstrated an elevated protein, otherwise unremarkable. Further serum and CSF testing was likewise negative for infectious or neoplastic etiologies, and demonstrated normal ACE levels. A high clinical suspicion remained for an underlying malignancy or sarcoidosis and a CT of the chest and abdomen was obtained. Follow up MRI after 6 weeks likewise demonstrated significant improvement and the patient was continued on their oral steroid taper.
Neurosarcoidosis frequently involves the leptomeninges but can also involve the hypothalamus, infundibulum, and cranial nerves. Neurosarcoidosis can follow an indolent course with marked variability in symptomology between patients. Clinically, patients may present with multiple cranial nerve deficits.
Generalized symptoms may include headache, fatigue, seizures, encephalopathy, cognitive deficits and psychiatric disturbances. This case demonstrates the utility of imaging studies in the diagnosis and treatment of this often overlooked condition. Side effects with panitumumab affecting the CNS beyond headache and dizziness, however, have not been reported so far. Upon neurologic examination she was comatose, had roving eyes, and bilateral Babinski signs. EEG did not show epileptiform activity. Conclusion: We conclude that acute encephalopathy may be a hitherto unrecognized complication of treatment with panitumumab and should be taken into consideration in patients developing CNS symptoms undergoing this therapy.
Direct interaction of the antibody with neuronal structures could be considered. Cerebral ischemia caused by paradoxical embolism, hyperviscosity, or other mechanism of action, however, cannot be completely ruled out.
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Eventually, pulmonary hypertension caused by deep vein thrombosis and subsequent embolism may have supported dislocation of the central line. Consistent with this hypothesis, we and others have demonstrated salient alterations in functional and structural connectivity in brain networks linking speech and language processing systems.
Magnetic stimuli were ms duration, at 0. Only one subject failed to show improvement on Day 10 compared to Day 1 after showing it on Day 5. These findings suggest that repeated bifocal mild magnetic stimulation of left perisylvian brain areas might be an effective treatment for DS. Few studies have identified significant impairments in phoneme discrimination after unilateral stroke. One study found that deficits in phoneme discrimination were seen in 14 percent of left hemisphere stroke patients acutely, and were associated with word comprehension deficits.
Lesion sites responsible for these deficits were not identified. Results: Twelve patients with completed testing had both DWI and perfusion imaging available at onset, to identify areas of acute tissue dysfunction. Seven patients had normal phoneme discrimination at all time points tested, and only one of these had hypoperfusion but no infarct in left STG.
Conclusion: Results show that left STG dysfunction is associated with phoneme discrimination deficits and auditory word comprehension deficits acutely, often due to hypoperfusion; and these deficits recover by 6 months if there is no infarct in left STG. Results also confirm that impaired phoneme discrimination may underlie at least some cases of word comprehension deficits. Autism spectrum disorder ASD is an increasingly common neurodevelopmental disorder with significant impairment of sensory behaviors. Despite identification of many genetic factors associated with ASD, the underlying neural circuit deficits remains poorly understood.
It has been suggested that imbalances in cortical excitation and inhibition may underlie ASD Rubenstein and Merzenich, Genes Brain Behavior, , but there is little consensus on how dysfunctional cortical excitatory and inhibitory neural activity impairs sensory behavior. By directly comparing neural population activity and visual behavior in normal versus CNTNAP2 mice, our goal is to identify how dysfunctional excitatory and inhibitory neural activity may directly contribute to sensory perception deficits in a genetically relevant mammalian ASD model.
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Mice learned to withhold from responding for a randomized period of time 0. We next performed multisite electrophysiological recordings in the primary visual cortex V1 during the behavioral task. Preliminary analysis suggests that the largest deficits are in the superficial feedforward layers of cortex. These preliminary findings identify a possible deficit of excitatory and inhibitory signaling that underlies deficits of sensory perception in a genetically relevant mouse model of ASD.
Our approach provides a path for further mechanistic understanding of neural circuit deficits underlying ASD. Subsequently, BK Ca channels can influence the shape, frequency and propagation of action potentials. They function as a powerful feedback mechanism, which regulates not only membrane potential but neurotransmitter release and therefore cortical circuit activity. Thus BK Ca channels may provide a potential therapeutic target for neurodevelopmental disorders. It has been suggested that the therapeutic effects of BMS may be mediated through normalization of brain connectivity abnormalities.
In consideration of the neurodevelopmental nature of FXS and the need for chronic treatment regimens, investigations exploring early critical periods for increased efficacy and daily dosing are crucial. We combined behavioral assessments with viral tracing approaches and whole brain clearing methods to investigate connectivity in the primary sensory cortices. We hypothesize that chronic treatment with BK Ca activators administered during early developmental periods rescues structural connectivity patterns of FXS mice. Our results provide a neurobiological substrate underlying the chronic effects of BMS.
Moreover, these data provide the first evidence regarding the critical role of early developmental time periods for the effects of BMS in a FXS model. This research provides insights in the etiopathological role and therapeutic potential of these channels in neurodevelopmental disorders. Introduction: Autoscopic mirror hallucinations have been described as virtual images of the person appearing outside the person, usually associated with a neurological condition involving the parietal or occipital lobes.
However, autoscopic hallucinations appearing only embedded in a mirror, has not heretofore been described. Such a case is presented. During these episodes, the autoscopic hallucination advises the patient in different ways through verbal communication. The patient's mouth does not move, but in the reflected image in the mirror the autoscopic hallucination's mouth is moving during its commands. As soon as the patient leaves the sight of a mirror, the visual and auditory hallucinations cease.
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In response to such distress, she pulls over to the side of the road to let the vehicle, the object of her delusion, drive away. Recent recall: 2 out of 4 objects with reinforcement. CN V: bilateral ptosis. CN X: absent gag reflex bilaterally. Reflexes: 0 in upper and lower extremities.
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Total protein: 8. Discussion: This patient demonstrated autoscopic hallucinations only when imbedded in a mirror. These context dependent hallucinations suggest a higher level of functioning since it approximates normal visual phenomena and is almost illusionary in nature.
The presence of this in an individual with fregoli syndrome implies a dysfunctional visual network for visual perception or recognition. While the brain tumor in this individual is not occipital or parietal in location, it may have induced secondary dysfunction to these regions as a result of diaschesis.