Dr. Juliana Lockman is Clinical Assistant Professor in the Neuropsychiatry Division in Department of Psychiatry & Behavioral Sciences at Stanford. She is also appointed to La Selva Group, where she directs the Functional Neurologic Symptom Disorder (FND) Track within their state-of-the-art residential, partial hospitalization and intensive outpatient programs. She completed residencies in both Neurology at the University of Virginia and Psychiatry at Stanford Hospital & Clinics. Her clinical activities include providing pharmacologic and behavioral care for clients with psychiatric and behavioral conditions in the context of neurological illness, including epilepsy, stroke, movement disorders and others. She also teaches and supervises Stanford residents and fellows in Neuropsychiatry. Professional goals include advancement of research and clinical care and improving access for clients suffering from neuropsychiatric conditions, including FND and related disorders.
Clinical Assistant Professor, Psychiatry and Behavioral Sciences
Boards, Advisory Committees, Professional Organizations
Member, American Neuropsychiatric Association (2016 - Present)
Member, National Alliance on Mental Illness (NAMI) (2015 - Present)
Member, American Psychiatric Association (2015 - Present)
Residency, Stanford Hospital and Clinics, Psychiatry (2018)
Fellowship, Stanford Hospital and Clinics, Epilepsy (2010)
Chief Residency, University of Virginia School of Medicine, Neurology (2008)
Residency, University of Virginia School of Medicine, Neurology (2007)
Internship, University of Virginia School of Medicine, Internal Medicine (2005)
M.D., University of Texas Health Science Center at San Antonio, Medical School (2004)
- Clinician Perceptions of Functional Neurological Symptom Disorder (FND): Outcome of a Cost-Effective Training Module. Abstract: 28th Annual Meeting of the American Neuropsychiatric Association
- The Effects of Group Psychodynamic Therapy on Psychological Characteristics and Psychogenic Non-Epileptic Seizure Frequency in Patients with Functional Neurological Symptom Disorder Abstract: 3rd International Conference on Functional (Psychogenic) Neurological Disorders. 2017
Ethical Considerations in Neuropsychiatric Disorders
2016; 14 (4)
View details for DOI 10.1176/appi.focus.20160021
Case Report: Rasmussen’s Encephalitis Treated Successfully with Rituximab
View details for DOI 10.7759/cureus.136
- Stiff Person Syndrome Netter Neurology Elsevier. 2012; 2nd
Detection of seizure-like movements using a wrist accelerometer
EPILEPSY & BEHAVIOR
2011; 20 (4): 638-641
Caregivers of people with epilepsy are commonly concerned about unwitnessed seizures causing injury and even death. The goal of this study was to determine if a wrist-worn motion detector could detect tonic-clonic seizures. Individuals admitted for continuous video/EEG monitoring wore a wristwatch-size device that was programmed to detect rhythmic movements such as those that occur during tonic-clonic seizures. When such movement was detected, the device sent a Bluetooth signal to a computer that registered the time and duration of the movements. Recorded detections were compared with the routinely recorded video/EEG data. Six of 40 patients had a total of eight tonic-clonic seizures. Seven of the eight seizures were detected. Nonseizure movements were detected 204 times, with opportunity for canceling transmission by the patient. Only one false detection occurred during sleep. In principle, this device should allow caregivers of people with tonic-clonic seizures to be alerted when a seizure occurs.
View details for DOI 10.1016/j.yebeh.2011.01.019
View details for PubMedID 21450533
Therapeutic Brain Stimulation for Epilepsy
2009; 27 (4): 1031-?
DBS has been a possible therapy for epilepsy for more than 30 years, and now it is moving to the point of clinical utility. Animal models have shown efficacy of DBS at several brain regions, although not all animal studies have shown efficacy. Clinically, an array of sites have been explored, including the cerebellum, anterior nucleus of the thalamus, CM nucleus, hippocampus, subthalamic nucleus, brainstem, and corpus callosum; direct stimulation of the cortex has also been explored. Interest in evaluating these sites for treatment of epilepsy has been enhanced by the success of vagus nerve stimulation for epilepsy and DBS for movement disorders. Literature consists of mostly small and uncontrolled studies that are subject to limitations in interpretation. A pivotal large, double-blind controlled trial of anterior nucleus of the thalamus has recently been completed, and it showed efficacy for partial seizures with or without secondary generalization.28 A controlled trial for RNS is underway.57 In addition, pilot studies of hippocampal stimulation 41,43 are expected to lead to more definitive trials of this site.Brain stimulation for epilepsy holds several challenges for the future. Mechanisms of DBS are poorly understood, although investigations are actively being pursued. Little is known about optimal stimulation parameters. DBS has been little examined in cases of intractable generalized epilepsy. Because DBS carries some risk, mainly of hemorrhage and infection, clinicians will need to develop an effective method of identifying the best candidates. DBS is palliative rather than curative, but experience suggests that this relatively new therapy may be of benefit to some people with otherwise untreatable epilepsy.
View details for DOI 10.1016/j.ncl.2009.06.005
View details for PubMedID 19853222
Current treatment options in neurology
2007; 9 (3): 234-240
Classic stiff-person syndrome (SPS) is a clinically diagnosed disease characterized by axial and often appendicular rigidity with lumbar hyperlordosis and painful spasms. Supportive data include increased glutamic acid decarboxylase autoantibody titers more than 20 nmol/L, a needle electromyography with continuous motor unit activity in at least one axial muscle, and normal MRI and cerebrospinal fluid studies. Variants of SPS include those with focal limb dysfunction (stiff-limb syndrome), encephalomyelitis ("SPS plus"), and those associated with paraneoplastic autoantibodies. Although the precise mechanism is unknown, an autoimmune etiology for SPS is proposed, based on its association with autoantibodies and other autoimmune diseases and its response to immunomodulatory therapy. The cornerstone of treatment consists of symptomatic care with benzodiazepines and/or baclofen. Other neuromodulators include antiepileptic medications and muscle relaxants. Continued disability despite first-line therapy should prompt consideration of agents aimed at immunomodulation and immunosuppression. Intravenous immunoglobulin is one of the few agents to be evaluated in a double-blind, randomized controlled trial. Other options include steroids, plasma exchange, and chemotherapy agents.
View details for PubMedID 17445501
Diplopia Due to Frontal Sinus Mucocele
ARCHIVES OF NEUROLOGY
2007; 64 (11)
View details for DOI 10.1001/archneur.64.11.1667
- Stiff-person syndrome Practical Neurology 2007; 7 (2)