Front Neurol

[Abigayle Laurenitis]

DrSantoro is a pediatric neurologist with special training in inflammatory and demyelinating disorders of the brain, spinal cord, and peripheral nervous system. His clinical research is in Down syndrome and the association between autoimmunity and the development of cerebrovascular disease.

Acute Disseminated Encephalomyelitis (ADEM)

Pediatric Multiple Sclerosis

Neuromyelitis Optica Spectrum Disorders

MOG Antibody Syndrome

Anti-NMDA Receptor Encephalitis

Optic Neuritis

Transverse Myelitis

Neurologic Disorders Associated With Down Syndrome

Bickerstaff's Brainstem Encephalitis and GQ1b Antibody Mediated Disorders

Autoimmune Encephalitis

Hashimoto's Encephalitis (Steroid Responsive Encephalitis with Associated Autoimmune Thyroiditis)

Down Syndrome Regression Disorder

Moyamoya vasculopathy

Aicardi Goutieres Syndrome

Dr. Guy Schwartz is trained to treat all neurological disorders. He is board certified in Neurology. He has special clinical interests in neurological movement disorders such as Parkinson's and Huntington's Disease.

Bocejo um comportamento estereotipado fisiolgico, o qual, contudo, pode representar um sinal ou sintoma de vrias condies neurolgicas, tais como, acidente vascular enceflico, incluindo a parakinesia brachial oscitans, parkinsonismo, doena de Parkinson, e epilepsia. Mais raramente, o bocejo pode ocorrer em pacientes com hipertenso intra-craniana, tumor cerebral, esclerose mltipla, migrnea, malformao de Chiari tipo I, e esclerose lateral amiotrfica. Bocejo-induzido por drogas representa outra condio clnica pouco comum. De outro modo, bocejo muito raro em pacientes com autismo e esquizofrenia. O objetivo desta reviso foi descrever em detalhes a ocorrncia deste fenmeno em tais condies, sua fenomenologia e fisiopatologia.

Yawning may occur not only because of boredom, drowsiness, or by contagion but also in association with various diseases. Yawning is termed pathological, abnormal, or excessive if it is spontaneous, more frequent than generally perceived as normal, compulsive, and not triggered by appropriate stimuli including fatigue or boredom. No consensus definition exists concerning the frequency of yawns. A recent recommendation adopted the abnormal yawning frequency as three yawns per 15 minutes to decrease the likelihood that two subsequent, accidental yawns were counted as one episode with abnormal yawning2323. Krestel H, Weisstanner C, Hess CW, Bassetti CL, Nirkko A, Wiest R. Insular and caudate lesions release abnormal yawning in stroke patients. Brain Struct Funct. 2015 Mar;220(2):803-12. -013-0684-6

-013-0684-... .

In general, excessive yawning occurs more frequently in patients with sleep disorders (e.g., insomnia and sleep obstructive apnea) and is most common in children and young adults1111. Walusinski O. Associated diseases. Front Neurol Neurosci. 2010;28:140-55.

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Other clinical conditions associated with yawning are functional digestive disorders (e.g., dyspepsia and irritable bowel syndrome), motion sickness and hypoglycemia in diabetic patients under insulin therapy1111. Walusinski O. Associated diseases. Front Neurol Neurosci. 2010;28:140-55.

. In addition, vasovagal syncopal or presyncopal episodes frequently present with yawning as well as malaise, dizziness, visual obscuration, nausea, pallor and loss of consciousness1111. Walusinski O. Associated diseases. Front Neurol Neurosci. 2010;28:140-55.

. Excessive yawning has also been reported in patients with depression and can be caused by the many medications used in neurology, psychiatry and internal medicine1111. Walusinski O. Associated diseases. Front Neurol Neurosci. 2010;28:140-55.

. This issue is discussed in the following section.

Dr. Quinn received a B.A. degree in Psychology (1998) from Princeton University. He earned his Doctor of Medicine degree (2004) from Harvard Medical School. Following his M.D. degree he completed a 4-year residency in Psychiatry at Massachusetts General Hospital/Mclean Hospital.

My current interests as an academic psychiatrist at the University of New Mexico include the cognitive, emotional, and behavioral manifestations of neurologic diseases and traumatic brain injury, the diagnosis and treatment of major depressive disorder in diverse populations, and the safe and effective use of neuromodulation therapies to treat psychiatric symptoms.

Following the conclusion of my fellowship training at Massachusetts General Hospital, I joined the UNM Department of Psychiatry in 2009, assumed medical directorship of the UNMH Psychiatric Consultation Service, and achieved board certification in adult psychiatry and consultation-liaison psychiatry. By applying evidence-based practice and ensuring high standards of consultation with a focus on helpfulness, I oversaw the near-doubling of the volume of the service. I founded the UNM/NMVAHCS Fellowship in Psychosomatic Medicine to train more specialists in consultation-liaison psychiatry, and have graduated seven CL psychiatrists. I formed and have served as Chief of the Division of Behavioral Health Consultation and Integration for the past four years, leading growth and expansion of psychiatric treatment in the areas of primary care, medical and surgical subspecialties, and at Sandoval Regional Medical Center. I am now the Vice Chair for Adult Clinical Services for the Department of Psychiatry and Behavioral Sciences. I have organized national conference symposia, written textbook chapters, and designed professional curricula in the areas of medical catatonia, traumatic brain injury, delirium, depression in kidney disease, noninvasive neuromodulation, and psychiatric complications in hepatitis C.

Owing to the large numbers of neurologically impaired patients requiring psychiatric consultation at UNM, I sought and achieved board certification in behavioral neurology/neuropsychiatry in 2012. I established a traumatic brain injury clinic co-located in the outpatient Neurosurgery Clinic to specifically address the needs of this population. In November of 2016 I became board-certified in brain injury medicine, and in my current outpatient practice I routinely handle neurobehavioral problems after TBI including agitation and impulsivity, executive dysfunction, and apathy. I am one of a small group of clinicians in the country who are board-certified in adult psychiatry, consultation psychiatry, behavioral neurology, and brain injury medicine.

My interest in neuromodulation began with my efforts to treat patients with severe neuropsychiatric syndromes after they failed to respond to pharmacotherapy. I have served as the Division Chief for Psychiatric Neuromodulation at UNM, as an attending on the Electroconvulsive Therapy (ECT) Service, and established the UNM Transcranial Magnetic Stimulation (TMS) Service in 2017. I treat patients clinically with ECT, TMS, vagal nerve stimulation, and deep brain stimulation. As a mentored PI in the UNM Center for Brain Recovery and Repair, I conducted a NIH/NIGMS-funded randomized controlled trial administering transcranial direct current stimulation (TDCS) to patients with mild to moderate TBI to ameliorate chronic cognitive and emotional deficits. I am now the consortium principal investigator for two multi-center Department of Defense-funded randomized controlled trials (NAVIGATE-TBI; CONNECT-TBI) examining targeted neuromodulation for deficits after TBI in US Veterans and Servicemembers using various advanced imaging modalities.

Dr. Raghupathi is a professor in the Department of Neurobiology & Anatomy at Drexel University College of Medicine. He did postdoctoral training at the University of Connecticut Health Science Center and the University of Pennsylvania School of Medicine. Before coming to the College of Medicine in 2003, he served on the faculty in the Department of Neurosurgery at the University of Pennsylvania School of Medicine.

The damage observed after TBI comprises both primary disruption of neural tissue related to the impact, and secondary mechanisms that develop over the weeks to months after the traumatic event. The spectrum of pathologies observed after TBI include focal contusions in the grey matter and diffuse injuries to axons in the white matter. It has been suggested that these pathologies are a consequence of the biomechanics of the impact, i.e., focal injuries occur due to contact forces to the head, while diffuse injuries are a result of non-contact, rotational forces to the brain. While aspects of focal pathology can be superimposed on diffuse brain injury (and vice versa), it is our belief that significant differences exist between the pathobiology of these two types of injuries that warrant the separate evaluation of mechanisms of damage in the cell body (soma) and the axon. Secondary mechanisms of neural damage are initiated immediately after impact and result in a number of cascades that affect both the neural tissue and the vasculature. In response to the impact, the brain becomes edematous leading to increases in intracranial pressure and subsequent neuronal death, which may be an underlying cause for the neurologic impairment. In turn, injured neurons are faced with imbalances in ionic homeostasis, over-activation of excitatory amino acid receptors, increases in intracellular calcium, increased free radical generation, and mitochondrial dysfunction that may underlie the eventual death of injured neurons. Concomitant with neuronal death and damage, axons are also subjected to mechanical forces that lead to traumatic axonal injury. Injury to axons is characterized by focal accumulations of cytoskeletal proteins resulting in a swollen phenotype in the acute post-traumatic period. Over time these swollen axons undergo complete axotomy (Wallerian degeneration), a process that is associated with death of oligodendrocytes.

The ongoing research efforts, funded in part by the National Institutes of Health and the Division of Veterans' Affairs, are aimed at addressing the feasibility of cellular and pharmacologic strategies to attenuate and reverse TBI pathology. The focus of the research in this group of investigators extend from the basic cell biology of neuronal death and axonal injury to inhibition of seizure induction to the behavioral and rehabilitative strategies (including neuro-robotics and prosthetic use) that may be applied in the chronic post-traumatic phase. The mission of the Raghupathi laboratory is to develop pharmacological treatment and behaviorally therapeutic strategies to, respectively, reduce acute post-traumatic neural damage and augment behavioral recovery in the chronic phase. Our research efforts offer some unique capabilities such as comparisons of acute and chronic pharmacologic treatments in multiple models of TBI, in both mice and rats, and, combination treatment strategies that encompass acute pharmacologic treatments with chronic phase behavioral modifications and/or stem cell transplants.

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